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宮本賢一

徳島大学

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2024年4月26日更新

職名: 名誉教授 (2020.4)
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学歴: 1989/1: 徳島大学大学院栄養学研究科(博士後期課程) 修了
学位: 保健学博士 (徳島大学) (1989年1月)
職歴・経歴: 〜: 徳島大学教授, 大学院ヘルスバイオサイエンス研究部 (-2015.3.)
2015/4: 徳島大学教授, 大学院医歯薬学研究部 (-2020.3.)

専門分野・研究分野: 保健学 (Health Studies)

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2024年4月26日更新

専門分野・研究分野: 保健学 (Health Studies)
担当経験のある授業科目: 研究者総覧に該当データはありませんでした。
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研究者総覧で最新データを確認する

2024年4月26日更新

専門分野・研究分野: 保健学 (Health Studies)

研究テーマ: 研究者総覧に該当データはありませんでした。

著書

辰巳佐和子, 野村憲吾, 釜谷達哉, 宮本賢一 :
ミネラル摂取と生命予後,
科学評論社, 宮本賢一 :
栄養素の構造と機能・遺伝子発現と栄養,
瀬川博子, 小池萌, 塩﨑雄治, 宮本賢一 :
抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性.,
2022年4月. 宮本賢一, 金子一郎 :
ロス医療栄養科学大事典7章カルシウム，8章リン,
西村書店, 2018年11月. 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 :
生体におけるリン代謝調節:多臓器連関について,
2018年10月. 花崎愛, 佐々木すみれ, 宮本賢一 :
リン.成人病と生活習慣病,
株式会社東京医学社, 2018年6月. 南久則, 宮本賢一, 山田耕路 :
消化管からみた健康・栄養,
株式会社建帛社, 2018年5月. 宮本賢一, 井上裕康, 桑波田雅士, 金子一郎 :
分子栄養学,
株式会社講談社, 2018年3月. 宮本賢一 :
グリコーゲンの合成と分解,
株式会社メディカ出版, 2017年4月. 宮本賢一 :
TCAサイクル(クエン酸回路),
株式会社メディカ出版, 2017年4月. 宮本賢一 :
ペントースリン酸回路,
株式会社メディカ出版, 2017年4月. 瀬川博子, 宮本賢一 :
Na+非依存性糖トランスポーターGLUT群の概要と糖輸送メカニズム.,
先端医学社, 2017年1月. 瀬川博子, 宮本賢一 :
腎臓とトランスポーター.,
医薬ジャーナル社, 2016年11月. 金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 :
尿細管リン再吸収障害によるくる病/骨軟化症.,
株式会社東京医学社, 2016年6月. 宮本賢一, 桑波田雅士 :
栄養素の代謝と生理機能.,
南江堂, 2016年6月. 宮川淳美, 金子一郎, 宮本賢一 :
栄養療法によるリン管理.,
医薬ジャーナル社, 2016年6月. 辰巳佐和子, 宮川敦美, 宮本賢一 :
新しいリン調節系,
中外医薬社, 2016年1月. 金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 :
FGF23,
科学評論社, 2015年12月. 生田かよ, 瀬川博子, 宮本賢一 :
りん吸収阻害薬の展望.,
株式会社東京医学社, 2015年9月. 藤井理, 宮本賢一 :
食事からの酸負荷と腸管吸収.,
株式会社東京医学社, 2015年8月. 大井彰子, 野村憲吾, 宮本賢一 :
リン摂取の危険性,
医薬ジャーナル社, 2015年3月. 辰巳佐和子, 宮本賢一 :
骨粗鬆症におけるカルシウムとリン摂取の考え方,
メディカルレビュー社, 2015年2月. 辰巳佐和子, 藤井理, 阪口晴菜, 緒方雅央, 新垣友啓, 宮本賢一 :
骨細胞の生理機能―骨細胞除去マウスの解析,
日本メディカルセンター, 2015年1月. 塩崎雄治, 宮本賢一 :
リンの栄養学―食物中のリンと食品添加物,
日本メディカルセンター, 2015年1月. 辰巳佐和子, 藤井理, 阪口晴菜, 緒方雅央, 新垣友啓, 宮本賢一 :
骨細胞の生理機能―骨細胞除去マウスの解析,
日本メディカルセンター., 2015年1月. 瀬川博子, 生田かよ, 宮本賢一 :
リンの吸収と排泄の分子機構,
医薬ジャーナル社, 2014年11月. 宮本賢一, 上畑陽子 :
腎臓病領域における専門栄養師育成―諸外国との比較検討―,
日本透析医会, 2014年11月. 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 :
生体内リン恒常性維持機構―多臓器関連制御,
日本DDS学会, 2014年11月. 宮本賢一 :
脂質の代謝と必要量,
株式会社中外医学社, 2014年8月. 佐々木祥平, 宮本賢一 :
タンパク質の代謝と栄養価(アミノ酸スコア),
株式会社中外医学社, 2014年8月. 塩崎雄治, 宮本賢一 :
糖質(炭水化物),
株式会社中外医学社, 2014年8月. 辰巳佐和子, 瀬川博子, 宮本賢一 :
骨のリン利尿因子,
医薬ジャーナル社, 2014年6月. 塩崎雄治, 宮本賢一 :
FGF23(骨分泌性繊維芽細胞増殖因子),
医学のあゆみ, 2014年5月. 大西律子, 佐々木祥平, 宮本賢一 :
リン代謝異常の病態・診断から治療まで,
文光堂, 2014年5月. 野村憲吾, 宮本賢一 :
リントランスポーターと疾患-リン代謝における骨と腎の相関-,
医歯薬出版株式会社, 2014年3月. 大西律子, 木戸慎介, 宮本賢一 :
慢性腎臓病におけるリン管理-リン添加物の話題.,
医歯薬出版株式会社, 2014年3月. 辰巳佐和子, 藤田みゆき, 野村憲吾, 藤井理, 宮本賢一 :
リン代謝と骨細胞.,
メディカルレビュー社, 2013年12月. 宮本賢一 :
知らずにとっているリン―リン添加物に注意―,
日本腎臓財団, 2013年11月. 瀬川博子, 大西沙織, 塩崎雄治, 佐々木祥平, 宮本賢一 :
リン輸送と疾患,
日本メディカルセンター, 2013年7月. 宮本賢一 :
尿細管トランスポーターと疾患―企画にあたって―,
日本メディカルセンター, 2013年7月. 瀬川博子, 宮本賢一 :
リンの吸収と排泄,
日本メディカルセンター, 2013年6月. 塩崎雄治, 野村憲吾, 宮本賢一 :
ミネラル代謝系の進化:海から陸,そして宇宙へ,
日本メディカルセンター, 2013年6月. 辰巳佐和子, 野村憲吾, 宮本賢一 :
骨細胞の機能と役割,
日本メディカルセンター, 2013年6月. 野村憲吾, 宮本賢一 :
リントランスポーターと疾患―リン代謝における骨と腎の相関―,
2013年4月. 辰巳佐和子, 木戸慎介, 宮本賢一, 伊藤美紀子 :
透析療法ネクストXIII∼新時代の高リン血症治療∼, --- 透析患者の栄養とリン代謝 ---,
医学図書出版株式会社, 埼玉, 2012年7月. 桑原頌治, 大井彰子, 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 :
消化と吸収Degestion&Absortion,
日本消化吸収学会, 2012年4月. 辰巳佐和子, 野村憲吾, 釜谷達哉, 宮本賢一 :
ミネラル摂取と生命予後,
科学評論社, 2012年3月. 坂井建雄, 宮本賢一, 小西真人, 工藤宏幸 :
人体の施錠構造と機能Ⅹ運動器,
2012年2月. 宮本賢一 :
動物を用いた栄養生化学および栄養関連酵素実験,
共立出版株式会社, 2012年1月. 伊藤美紀子, 宮本賢一, 辰巳佐和子 :
栄養不良の定義,
日本メディカルセンター, 2011年6月. 桑原頌治, 西山俊, 大井彰子, 金子一郎, 辰巳佐和子, 伊藤美紀子, 竹谷豊, 宮本賢一 :
リン酸トランスポーター関連分子群とリン代謝異常症,
メディカルドゥ社, 2011年3月. 宮本賢一, 竹谷豊, 辰巳佐和子, 伊藤美紀子, 瀬川博子 :
無機リン酸イオンとトランスポーター,
京都廣川書店, 2011年3月. 宮本賢一, 桑波田雅士 :
栄養素の代謝と生理機能,
メディカルレビュー社, 2011年1月. 宮本賢一, 古谷順也 :
ペプチド輸送におけるペプチドトランスポーターの役割,
けんぱく社, 東京, 2010年5月. 宮本賢一, 瀬川博子 :
リントランスポーター,
株式会社先端医学社, 2010年4月. 宮本賢一, 瀬川博子 :
リントランスポーター,
2010年4月. 中屋豊, 宮本賢一, 坂巻路可, 乾明夫, 合田敏尚, 南久則, 川崎英二, 長田恭一, 佐藤隆一郎, 長澤孝志, 渡邊文雄, 岡達三, 桑波田雅士, 髙橋章, 竹谷豊 :
エッセンシャル基礎栄養学,
医歯薬出版株式会社, 東京, 2005年11月. 森田秀芳, 桑折範彦, 高石喜久, 廣渡修一, 宮本賢一 :
授業改善のための授業研究会運営ハンドブック, --- 徳島大学FD推進ハンドブック第4巻 ---,
大学開放実践センター, 徳島, 2002年12月. 宮本賢一, 伊藤美紀子 :
リン代謝調節系とその異常,
株式会社中外医学社, 2002年5月. 伊藤美紀子, 瀬川博子, 桑波田雅士, 宮本賢一 :
無機リン酸トランスポーターファミリー,
株式会社中外医学社, 2002年1月.

(キーワード): Renal Phosphate Transporter / Parathyroid Hormone / Endocytosis / PDZ Domain / Brush Border Membrane

宮本賢一, 伊藤美紀子, 瀬川博子, 徳永栄子 :
ビタミンD輸送システムと結合蛋白,
2001年.

論文

Megumi Koike, Tetsuhiko Sato, Yuji Shiozaki, Aoi Komiya, Mizuki Miura, Ayami Higashi, Akane Ishikawa, Kaori Takayanagi, Minori Uga, Ken-ichi Miyamoto and Hiroko Segawa :
Involvement of α-klotho in growth hormone (GH) signaling,
Journal of Clinical Biochemistry and Nutrition, 2024. Kazuya Tanifuji, Yuji Shiozaki, Megumi Koike, Minori Uga, Mizuki Miura, Ayami Higashi, Takaaki Shimohata, Akira Takahashi, Hisayoshi Hayashi, Noriko Ishizuka, Yasuhiro Ichida, Shuichi Ohtomo, Naoshi Horiba, Ken-ichi Miyamoto and Hiroko Segawa :
Effects of EOS789, a novel pan-phosphate transporter inhibitor, on phosphate metabolism : Comparison with a conventional phosphate binder,
The Journal of Medical Investigation : JMI, Vol.70, No.1,2, 260-270, 2023.

(要約): Inorganic phosphate (Pi) binders are the only pharmacologic treatment approved for hyperphosphatemia. However, Pi binders induce the expression of intestinal Pi transporters and have limited effects on the inhibition of Pi transport. EOS789, a novel pan-Pi transporter inhibitor, reportedly has potent efficacy in treating hyperphosphatemia. We investigated the properties of EOS789 with comparison to a conventional Pi binder. Protein and mRNA expression levels of Pi transporters were measured in intestinal and kidney tissues from male Wistar rats fed diets supplemented with EOS789 or lanthanum carbonate (LC). 32Pi permeability was measured in intestinal tissues from normal rats using a chamber. Increased protein levels of NaPi-2b, an intestinal Pi transporter, and luminal Pi removal were observed in rats treated with LC but not in rats treated with EOS789. EOS789 but not LC suppressed intestinal protein levels of the Pi transporter Pit-1 and sodium/hydrogen exchanger isoform 3. 32Pi flux experiments using small intestine tissues from rats demonstrated that EOS789 may affect transcellular Pi transport in addition to paracellular Pi transport. EOS789 has differing regulatory effects on Pi metabolism compared to LC. The properties of EOS789 may compensate for the limitations of LC therapy. The combined or selective use of EOS789 and conventional Pi binders may allow tighter control of hyperphosphatemia. J. Med. Invest. 70 : 260-270, February, 2023.
(キーワード): Rats / Male / Animals / Phosphate Transport Proteins / Rats, Wistar / Hyperphosphatemia / Intestinal Absorption / Phosphates
(徳島大学機関リポジトリ): ● Metadata: 118209
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.70.260
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164731; ● Search Scopus @ Elsevier (PMID): 37164731; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.260

(徳島大学機関リポジトリ: 118209, DOI: 10.2152/jmi.70.260, PubMed: 37164731) Sumire Sasaki, Yuji Shiozaki, Ai Hanazaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Ichiro Kaneko, Yasuharu Kawamoto, Pattama Wiriyasermkul, Tomoka Hasegawa, Norio Amizuka, Ken-ichi Miyamoto, Shushi Nagamori, Yoshikatsu Kanai and Hiroko Segawa :
Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia.,
Scientific Reports, Vol.12, No.1, 2022.

(要約): Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces expression and secretion of the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) that enhance urinary Pi excretion and prevent the onset of hyperphosphatemia. How FGF23 secretion from bone is increased by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of Transmembrane protein 174 (Tmem174) and observed evidence for gene co-expression networks in NaPi2a and NaPi2c function. Tmem174 is localized in the renal proximal tubules and interacts with NaPi2a, but not NaPi2c. In Tmem174-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, Tmem174-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in Tmem174-KO mice. Thus, Tmem174 is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury.
(キーワード): Animals / Fibroblast Growth Factors / 高リン血症 (hyperphosphatemia) / 低リン血症 (hypophosphatemia) / Membrane Proteins / ノックアウトマウス (knockout mice) / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-022-10409-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35428804; ● Search Scopus @ Elsevier (PMID): 35428804; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-10409-3

(DOI: 10.1038/s41598-022-10409-3, PubMed: 35428804) Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Aoi Komiya, Mizuki Miura, Yamato Harada, Yuki Hamaguchi, Shohei Sasaki, Yuji Shiozaki, Ichiro Kaneko, Ken-ichi Miyamoto and Hiroko Segawa :
Dietary polyphosphate has a greater effect on renal damage and FGF23 secretion than dietary monophosphate,
The Journal of Medical Investigation : JMI, Vol.69, No.3, 173-179, 2022.

(要約): Phosphate (Pi)-containing food additives are used in several forms. Polyphosphate (PPi) salt has more harmful effects than monophosphate (MPi) salt on bone physiology and renal function. This study aimed to analyze the levels of parathyroid hormone PTH and fibroblast growth factor 23 (FGF23) and the expression of renal / intestinal Pi transport-related molecules in mice fed with an MPi or PPi diet. There were no significant differences in plasma Pi concentration and fecal Pi excretion levels between mice fed with the high-MPi and PPi diet. However, more severe tubular dilatation, interstitial fibrosis, and calcification were observed in the kidneys of mice fed with the high PPi diet versus the MPi diet. Furthermore, there was a significant increase in serum FGF23 levels and a decrease in renal phosphate transporter protein expression in mice fed with the PPi diet versus the MPi diet. Furthermore, the high MPi diet was associated with significantly suppressed expression and activity of intestinal alkaline phosphatase protein. In summary, PPi has a more severe effect on renal damage than MPi, as well as induces more FGF23 secretion. Excess FGF23 may be more involved in inflammation, fibrosis, and calcification in the kidney. J. Med. Invest. 69 : 173-179, August, 2022.
(キーワード): Animals / Mice / Alkaline Phosphatase / Diet / Fibroblast Growth Factors / Fibrosis / Food Additives / Kidney / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates / Polyphosphates
(徳島大学機関リポジトリ): ● Metadata: 117148
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.69.173
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244766; ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886601

(徳島大学機関リポジトリ: 117148, DOI: 10.2152/jmi.69.173, PubMed: 36244766, Elsevier: Scopus) Toru Fujii, Hiroko Segawa, Ai Hanazaki, Shiori Nishiguchi, Sakura Minoshima, Akiko Ohi, Rieko Tominaga, Sumire Sasaki, Kazuya Tanifuji, Megumi Koike, Yuki Arima, Yuji Shiozaki, Ichiro Kaneko, Mikiko Ito, Sawako Tatsumi and Ken-ichi Miyamoto :
Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation.,
Clinical and Experimental Nephrology, Vol.23, No.7, 898-907, 2019.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-019-01725-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30895530; ● Search Scopus @ Elsevier (PMID): 30895530; ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-019-01725-6

(DOI: 10.1007/s10157-019-01725-6, PubMed: 30895530) Kayo Ikuta, Hiroko Segawa, Ai Hanazaki, Toru Fujii, Ichiro Kaneko, Yuji Shiozaki, Sawako Tatsumi, Yasuko Ishikawa and Ken-ichi Miyamoto :
Systemic network for dietary inorganic phosphate adaptation among three organs.,
Pflügers Archiv : European Journal of Physiology, Vol.471, No.1, 123-136, 2018.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00424-018-2242-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30523405; ● Search Scopus @ Elsevier (PMID): 30523405; ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-018-2242-9

(DOI: 10.1007/s00424-018-2242-9, PubMed: 30523405) Toru Fujii, Yuji Shiozaki, Hiroko Segawa, Shiori Nishiguchi, Ai Hanazaki, Miwa Noguchi, Ruri Kirino, Sumire Sasaki, Kazuya Tanifuji, Megumi Koike, Mizuki Yokoyama, Yuki Arima, Ichiro Kaneko, Sawako Tatsumi, Mikiko Ito and Ken-ichi Miyamoto :
Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney.,
Clinical and Experimental Nephrology, Vol.23, No.3, 313-324, 2018.

(キーワード): Animals / Cells, Cultured / Familial Hypophosphatemic Rickets / Humans / Hypercalciuria / Kidney / Mice / Opossums / Phosphate Transport Proteins / Phosphates / RNA, Small Interfering / Sodium-Phosphate Cotransporter Proteins, Type IIc / Xenopus laevis
(徳島大学機関リポジトリ): ● Metadata: 113363
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-018-1653-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30317447; ● Search Scopus @ Elsevier (PMID): 30317447; ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-018-1653-4

(徳島大学機関リポジトリ: 113363, DOI: 10.1007/s10157-018-1653-4, PubMed: 30317447) Shohei Sasaki, Hiroko Segawa, Ai Hanazaki, Ruri Kirino, Toru Fujii, Kayo Ikuta, Miwa Noguchi, Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Yuji Shiozaki, Ichiro Kaneko, Sawako Tatsumi, Takaaki Shimohata, Yoshichika Kawai, Sonoko Narisawa, Luis José Millán and Ken-ichi Miyamoto :
A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis.,
Kidney & Blood Pressure Research, Vol.43, No.5, 1409-1424, 2018.

(キーワード): Alkaline Phosphatase / Animals / Biological Transport / Disease Models, Animal / Homeostasis / Intestinal Mucosa / Mice / Mice, Knockout / Phosphates / Renal Insufficiency / Sodium-Phosphate Cotransporter Proteins, Type IIb
(徳島大学機関リポジトリ): ● Metadata: 112882
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000493379
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30212831; ● Search Scopus @ Elsevier (PMID): 30212831; ● Search Scopus @ Elsevier (DOI): 10.1159/000493379

(徳島大学機関リポジトリ: 112882, DOI: 10.1159/000493379, PubMed: 30212831) Ichiro Kaneko, Hiroko Segawa, Ikuta Kayo, Hanazaki Ai, Fujii Toru, Sawako Tatsumi, Kido Shinsuke, Hasegawa Tomoka, Amizuka Norio, Saito Hitoshi and Ken-ichi Miyamoto :
Eldecalcitol Causes FGF23 Resistance for Pi Reabsorption and Improves Rachitic Bone Phenotypes in the Male Hyp Mouse.,
Endocrinology, Vol.159, No.7, 2741-2758, 2018.

(要約): X-linked hypophosphatemia (XLH), the most common form of inheritable rickets, is caused by inactivation of phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) and leads to fibroblast growth factor (FGF) 23-dependent renal inorganic phosphate (Pi) wasting. In the present study, we investigated whether maintaining Pi homeostasis with a potent vitamin D3 analog, eldecalcitol [1α,25-dihydroxy-2β-(3-hydroxypropyloxy) vitamin D3; ED71], could improve hypophosphatemic rickets in a murine model of XLH, the Hyp mouse. Vehicle, ED71, or 1,25-dihydroxyvitamin D was subcutaneously injected five times weekly in wild-type (WT) and Hyp mice for 4 weeks, from 4 to 8 weeks of age. Injection of ED71 into WT mice suppressed the synthesis of renal 1,25-dihydroxyvitamin D and promoted phosphaturic activity. In contrast, administration of ED71 to Hyp mice completely restored renal Pi transport and NaPi-2a protein levels, although the plasma-intact FGF23 levels were further increased. In addition, ED71 markedly increased the levels of the scaffold proteins, renal sodium-hydrogen exchanger regulatory factor 1, and ezrin in the Hyp mouse kidney. Treatment with ED71 increased the body weight and improved hypophosphatemia, the bone volume/total volume, bone mineral content, and growth plate structure in Hyp mice. Thus, ED71 causes FGF23 resistance for phosphate reabsorption and improves rachitic bone phenotypes in Hyp mice. In conclusion, ED71 has opposite effects on phosphate homeostasis in WT and Hyp mice. Analysis of Hyp mice treated with ED71 could result in an additional model for elucidating PHEX abnormalities.
(出版サイトへのリンク): ● Publication site (DOI): 10.1210/en.2018-00109
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29878089; ● Search Scopus @ Elsevier (PMID): 29878089; ● Search Scopus @ Elsevier (DOI): 10.1210/en.2018-00109

(DOI: 10.1210/en.2018-00109, PubMed: 29878089) Atsumi Miyagawa, Sawako Tatsumi, Wako Takahama, Osamu Fujii, Kenta Nagamoto, Emi Kinoshita, Kengo Nomura, Kayo Ikuta, Toru Fujii, Ai Hanazaki, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
The sodium phosphate cotransporter family and nicotinamide phosphoribosyltransferase contribute to the daily oscillation of plasma inorganic phosphate concentration.,
Kidney International, Vol.93, No.5, 1073-1085, 2018.

(要約): system for Npt2 regulation and cellular shifts to tissues such as the liver play an important role in generating daily oscillation of plasma inorganic phosphate levels.
(徳島大学機関リポジトリ): ● Metadata: 111600
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.kint.2017.11.022
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29398136; ● Search Scopus @ Elsevier (PMID): 29398136; ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2017.11.022

(徳島大学機関リポジトリ: 111600, DOI: 10.1016/j.kint.2017.11.022, PubMed: 29398136) Osamu Fujii, Sawako Tatsumi, Mao Ogata, Tomohiro Arakaki, Haruna Sakaguchi, Kengo Nomura, Atsumi Miyagawa, Kayo Ikuta, Ai Hanazaki, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
Effect of Osteocyte-Ablation on Inorganic Phosphate Metabolism: Analysis of Bone-Kidney-Gut Axis.,
Frontiers in Endocrinology, Vol.8, 2017.

(要約): < 0.01), thus suggesting that increased intestinal Pi absorption stimulates renal Pi excretion in OCL mice. In addition, the ablation of osteocytes and feeding of a high Pi diet affected FGF15/bile acid metabolism and controlled Npt2b expression. In conclusion, OCL mice exhibited increased renal Pi excretion due to enhanced intestinal Pi absorption. We discuss the role of FGF23-Klotho on renal and intestinal Pi metabolism in OCL mice.
(徳島大学機関リポジトリ): ● Metadata: 112958
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fendo.2017.00359
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29312149; ● Search Scopus @ Elsevier (PMID): 29312149; ● Search Scopus @ Elsevier (DOI): 10.3389/fendo.2017.00359

(徳島大学機関リポジトリ: 112958, DOI: 10.3389/fendo.2017.00359, PubMed: 29312149) Kayo Ikuta, Hiroko Segawa, Shohei Sasaki, Ai Hanazaki, Toru Fujii, Aoi Kushi, Yuka Kawabata, Ruri Kirino, Sumire Sasaki, Miwa Noguchi, Ichiro Kaneko, Sawako Tatsumi, Otoya Ueda, Naoko Wada, Hiromi Tateishi, Mami Kakefuda, Yosuke Kawase, Shuichi Ohtomo, Yasuhiro Ichida, Akira Maeda, Kou-Ichi Jishage, Naoshi Horiba and Ken-ichi Miyamoto :
Effect of Npt2b deletion on intestinal and renal inorganic phosphate (Pi) handling.,
Clinical and Experimental Nephrology, Vol.22, No.3, 517-528, 2017.

(要約): -dependent Pi transport in brush-border membrane vesicle uptake levels was significantly decreased in the distal intestine of Npt2b CKO mice compared with control mice, plasma Pi and fecal Pi excretion levels were not significantly different. Data obtained using the intestinal loop technique showed that Pi uptake in Npt2b CKO mice was not affected at a Pi concentration of 4 mM, which is considered the typical luminal Pi concentration after meals in mice. Claudin, which may be involved in paracellular pathways, as well as claudin-2, 12, and 15 protein levels were significantly decreased in the Npt2b CKO mice. Thus, Npt2b deficiency did not affect Pi absorption within the range of Pi concentrations that normally occurs after meals.
(徳島大学機関リポジトリ): ● Metadata: 111601
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-017-1497-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29128884; ● Search Scopus @ Elsevier (PMID): 29128884; ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-017-1497-3

(徳島大学機関リポジトリ: 111601, DOI: 10.1007/s10157-017-1497-3, PubMed: 29128884) Sawako Tatsumi, A Miyagawa, Ichiro Kaneko, Y Shiozaki, Hiroko Segawa and Ken-ichi Miyamoto :
Regulation of renal phosphate handling: inter-organ communication in health and disease.,
Journal of Bone and Mineral Metabolism, Vol.34, No.1, 1-10, 2016.

(要約): In this review, we focus on the interconnection of inorganic phosphate (Pi) homeostasis in the network of the bone-kidney, parathyroid-kidney, intestine-kidney, and liver-kidney axes. Such a network of organ communication is important for body Pi homeostasis. Normalization of serum Pi levels is a clinical target in patients with chronic kidney disease (CKD). Particularly, disorders of the fibroblast growth factor 23/klotho system are observed in early CKD. Identification of phosphaturic factors from the intestine and liver may enhance our understanding of body Pi homeostasis and Pi metabolism disturbances in CKD patients.
(キーワード): Bone and Bones / Homeostasis / Humans / Intestines / Kidney / Liver / Parathyroid Glands / Phosphates / Renal Insufficiency, Chronic
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00774-015-0705-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26296817; ● Search Scopus @ Elsevier (PMID): 26296817; ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-015-0705-z

(DOI: 10.1007/s00774-015-0705-z, PubMed: 26296817) Ken-ichi Miyamoto, Sawako Tatsumi and Yasuhiro Hamada :
Clinical Nutrition education in Japanese dietitians,
第60回日本透析医学会, 2015. Yuji Shiozaki, Hiroko Segawa, Saori Ohnishi, Akiko Ohi, Mikiko Ito, Ichiro Kaneko, Shinsuke Kido, Sawako Tatsumi and Ken-ichi Miyamoto :
Relationship between sodium-dependent phosphate transporter (NaPi-IIc) function and cellular vacuole formation in opossum kidney cells.,
The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 209-218, 2015.

(要約): NaPi-IIc/SLC34A3 is a sodium-dependent inorganic phosphate (Pi) transporter in the renal proximal tubules and its mutations cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH). In the present study, we created a specific antibody for opossum SLC34A3, NaPi-IIc (oNaPi-IIc), and analyzed its localization and regulation in opossum kidney cells (a tissue culture model of proximal tubular cells). Immunoreactive oNaPi-IIc protein levels increased during the proliferative phase and decreased during differentiation. Moreover, stimulating cell growth upregulated oNaPi-IIc protein levels, whereas suppressing cell proliferation downregulated oNaPi-IIc protein levels. Immunocytochemistry revealed that endogenous and exogenous oNaPi-IIc proteins localized at the protrusion of the plasma membrane, which is a phosphatidylinositol 4,5-bisphosphate (PIP2) rich-membrane, and at the intracellular vacuolar membrane. Exogenous NaPi-IIc also induced cellular vacuoles and localized in the plasma membrane. The ability to form vacuoles is specific to electroneutral NaPi-IIc, and not electrogenic NaPi-IIa or NaPi-IIb. In addition, mutations of NaPi-IIc (S138F and R468W) in HHRH did not cause cellular PIP2-rich vacuoles. In conclusion, our data anticipate that NaPi-IIc may regulate PIP2 production at the plasma membrane and cellular vesicle formation.
(徳島大学機関リポジトリ): ● Metadata: 111281
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.62.209
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399350; ● Summary page in Scopus @ Elsevier: 2-s2.0-84942042069

(徳島大学機関リポジトリ: 111281, DOI: 10.2152/jmi.62.209, PubMed: 26399350, Elsevier: Scopus) Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Hiroko Segawa, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto :
Niacin and Chronic Kidney Disease.,
Journal of Nutritional Science and Vitaminology, Vol.61 Suppl, S173-5, 2015.

(要約): Chronic kidney disease (CKD) is an increasing problem worldwide. The number of end-stage renal disease patients requiring treatment by dialysis is estimated to be increasing by 10,000 patients per year in Japan. Furthermore, an estimated 13 million people are living with CKD in Japan. Various complications are associated with CKD, including cardiovascular disease (CVD). More than one-third of CKD patients die from CVD. Thus, prevention of CVD is a primary concern for the treatment of CKD patients. CKD-mineral and bone disorder (CKD-MBD) is a serious complication that typically leads to CVD. Hyperphosphatemia is thought to be a central-risk factor for CKD-MBD. Therefore, managing hyperphosphatemia is crucial to prevent CKD-MBD and CVD. It is difficult to achieve the target serum phosphate level through dietary modifications alone in patients with hyperphosphatemia, because most foods contain phosphate. Thus, phosphate binders such as calcium carbonate are commonly prescribed to CKD patients with hyperphosphatemia, but these have undesirable side effects. Inhibition of intestinal phosphate transport activity has also been investigated as an alternative approach for controlling serum phosphate levels in CKD patients. Nicotinamide, which is the amide of niacin, can inhibit intestinal phosphate transport. Niacin and related compounds have also been developed as drugs for hyperlipidemia conditions, especially hypertriglyceridemia with low high-density lipoprotein. This type of dyslipidemia is frequently observed in CKD patients and is a modifiable risk factor for CVD. Thus, niacin and related compounds may have utility for the treatment of both hyperphosphatemia and dyslipidemia in CKD patients to prevent CVD.
(出版サイトへのリンク): ● Publication site (DOI): 10.3177/jnsv.61.S173
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26598845; ● Summary page in Scopus @ Elsevier: 2-s2.0-84950314636

(DOI: 10.3177/jnsv.61.S173, PubMed: 26598845, Elsevier: Scopus) Kengo Nomura, Sawako Tatsumi, Atsumi Miyagawa, Yuji Shiozaki, Shohei Sasaki, Ichiro Kaneko, Mikiko Ito, Shinsuke Kido, Hiroko Segawa, Mitsue Sano, Tsutomu Fukuwatari, Katsumi Shibata and Ken-ichi Miyamoto :
Hepatectomy-related hypophosphatemia: a novel phosphaturic factor in the liver-kidney axis.,
Journal of the American Society of Nephrology, Vol.25, No.4, 761-772, 2014.

(要約): Marked hypophosphatemia is common after major hepatic resection, but the pathophysiologic mechanism remains unknown. We used a partial hepatectomy (PH) rat model to investigate the molecular basis of hypophosphatemia. PH rats exhibited hypophosphatemia and hyperphosphaturia. In renal and intestinal brush-border membrane vesicles isolated from PH rats, Na(+)-dependent phosphate (Pi) uptake decreased by 50%-60%. PH rats also exhibited significantly decreased levels of renal and intestinal Na(+)-dependent Pi transporter proteins (NaPi-IIa [NaPi-4], NaPi-IIb, and NaPi-IIc). Parathyroid hormone was elevated at 6 hours after PH. Hyperphosphaturia persisted, however, even after thyroparathyroidectomy in PH rats. Moreover, DNA microarray data revealed elevated levels of nicotinamide phosphoribosyltransferase (Nampt) mRNA in the kidney after PH, and Nampt protein levels and total NAD concentration increased significantly in the proximal tubules. PH rats also exhibited markedly increased levels of the Nampt substrate, urinary nicotinamide (NAM), and NAM catabolites. In vitro analyses using opossum kidney cells revealed that NAM alone did not affect endogenous NaPi-4 levels. However, in cells overexpressing Nampt, the addition of NAM led to a marked decrease in cell surface expression of NaPi-4 that was blocked by treatment with FK866, a specific Nampt inhibitor. Furthermore, FK866-treated mice showed elevated renal Pi reabsorption and hypophosphaturia. These findings indicate that hepatectomy-induced hypophosphatemia is due to abnormal NAM metabolism, including Nampt activation in renal proximal tubular cells.
(キーワード): Acrylamides / Animals / Hepatectomy / Hypophosphatemia / Kidney / Male / Mice / Mice, Inbred C57BL / NAD / Niacinamide / Nicotinamide Phosphoribosyltransferase / Parathyroidectomy / Piperidines / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa
(徳島大学機関リポジトリ): ● Metadata: 106156
(出版サイトへのリンク): ● Publication site (DOI): 10.1681/ASN.2013060569
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24262791; ● Search Scopus @ Elsevier (PMID): 24262791; ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.2013060569

(徳島大学機関リポジトリ: 106156, DOI: 10.1681/ASN.2013060569, PubMed: 24262791) Shinsuke Kido, Marina Fujihara, Kengo Nomura, Shohei Sasaki, Rie Mukai, Ritsuko Ohnishi, Ichiro Kaneko, Hiroko Segawa, Sawako Tatsumi, Hiroto Izumi, Kimitoshi Kohno and Ken-ichi Miyamoto :
Molecular mechanisms of cadmium-induced fibroblast growth factor 23 upregulation in osteoblast-like cells.,
Toxicological Sciences, Vol.139, No.2, 301-316, 2014.

(要約): Itai-itai disease is thought to be the result of chronic cadmium (Cd) intoxication. Renal proximal tubules are a major target of Cd toxicity. The whole mechanism of the adverse effects of Cd remains unresolved, especially how renal damage is related to the development of bone lesions. Fibroblast growth factor 23 (FGF23) is a bone-derived phosphaturic factor that regulates vitamin D and inorganic phosphate metabolism in the kidney. To clarify the role of FGF23 on Cd toxicity, we investigated the mechanisms of Cd-induced FGF23 production in the bone. Cd injection into mice significantly increased plasma FGF23 concentrations, but did not change FGF23 mRNA expression in bone. GalNAc-T3 is involved in secreting intact FGF23. To determine potential roles of GalNAc-T3 in Cd-induced FGF23 production, we examined the effect of Cd on GalNAc-T3 mRNA expression in vivo and in vitro. GalNAc-T3 gene expression was significantly increased in the bones of Cd-injected mice. Cd also enhanced the expression of GalNAc-T3 in cultured osteosarcoma UMR106 cells and primary osteocytes. Cd activated aryl hydrocarbon receptors (AhR) and AhR were required for GalNAc-T3 gene expression induced by Cd. In addition, Cd-dependent FGF23 production was completely inhibited by an AhR antagonist. AhR siRNA markedly suppressed the stimulation of transcriptional activity by Cd. Furthermore, Cd induced AhR activation via phosphorylation of Ser-68 by p38 kinase in the nuclear export signal of AhR. Thus, Cd stimulated GalNAc-T3 gene transcription via enhanced AhR binding to the GalNAc-T3 promoter. These findings suggest that the Cd-induced increase in GalNAc-T3 suppresses proteolytic processing of FGF23 and increases serum FGF23 concentrations.
(キーワード): Animals / Cadmium Chloride / Cell Culture Techniques / Cell Line, Tumor / Female / Femur / Fibroblast Growth Factors / Gene Expression / Mice, Inbred C57BL / Mice, Inbred ICR / N-Acetylgalactosaminyltransferases / Osteoblasts / Osteocytes / Phosphorylation / Receptors, Aryl Hydrocarbon / Up-Regulation / p38 Mitogen-Activated Protein Kinases
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/toxsci/kfu043
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24614234; ● Summary page in Scopus @ Elsevier: 2-s2.0-84899983795

(DOI: 10.1093/toxsci/kfu043, PubMed: 24614234, Elsevier: Scopus) Otoki Nakahashi, Hironori Yamamoto, Sarasa Tanaka, Mina Kozai, Yuichiro Takei, Masashi Masuda, Ichiro Kaneko, Yutaka Taketani, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda :
Short-term dietary phosphate restriction up-regulates ileal fibroblast growth factor 15 gene expression in mice.,
Journal of Clinical Biochemistry and Nutrition, Vol.54, No.2, 102-108, 2014.

(要約): Members of the fibroblast growth factor (FGF) 19 subfamily, including FGF23, FGF15/19, and FGF21, have a role as endocrine factors which influence the metabolism of inorganic phosphate (Pi) and vitamin D, bile acid, and energy. It has been reported that dietary Pi regulates circulating FGF23. In this study, the short-term effects of dietary Pi restriction on the expression of FGF19 subfamily members in mice were analyzed. An initial analysis confirmed plasma FGF23 levels positively correlated with the amount of dietary Pi. On the other hand, ileal Fgf15 gene expression, but not hepatic Fgf21 gene expression, was up-regulated by dietary Pi restriction. In addition, we observed the increase of plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels by dietary Pi restriction, and the up-regulation of ileal Fgf15 mRNA expression by 1,25(OH)2D3 and vitamin D receptor (VDR). Importantly, dietary Pi restriction-induced Fgf15 gene expression was prevented in VDR-knockout mice. Furthermore, diurnal variations of plasma triglyceride concentrations and hepatic mRNA expression of the bile acid synthesis enzyme Cyp7a1 as one of Fgf15 negative target genes was influenced by dietary Pi restriction. These results suggest that dietary Pi restriction up-regulates ileal Fgf15 gene expression through 1,25(OH)2D3 and VDR, and may affect hepatic bile acid homeostasis.
(徳島大学機関リポジトリ): ● Metadata: 106159
(出版サイトへのリンク): ● Publication site (DOI): 10.3164/jcbn.13-109
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24688219; ● Search Scopus @ Elsevier (PMID): 24688219; ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.13-109

(徳島大学機関リポジトリ: 106159, DOI: 10.3164/jcbn.13-109, PubMed: 24688219) Shoko Ikeda, Hironori Yamamoto, Masashi Masuda, Yuichiro Takei, Otoki Nakahashi, Mina Kozai, Sarasa Tanaka, Mari Nakao, Yutaka Taketani, Hiroko Segawa, Masayuki Iwano, Ken-ichi Miyamoto and Eiji Takeda :
Downregulation of renal type IIa sodium-dependent phosphate cotransporter during lipopolysaccharide-induced acute inflammation.,
American Journal of Physiology, Renal Physiology, Vol.306, No.7, F744-50, 2014.

(要約): The type IIa sodium-dependent phosphate cotransporter (Npt2a) plays a critical role in reabsorption of inorganic phosphate (Pi) by renal proximal tubular cells. Pi abnormalities during early stages of sepsis have been reported, but the mechanisms regulating Pi homeostasis during acute inflammation are poorly understood. We examined the regulation of Pi metabolism and renal Npt2a expression during lipopolysaccharide (LPS)-induced inflammation in mice. Dose-response and time-course studies with LPS showed significant increases of plasma Pi and intact parathyroid hormone (iPTH) levels and renal Pi excretion, while renal calcium excretion was significantly decreased. There was no difference in plasma 1,25-dihydroxyvitamin D levels, but the induction of plasma intact fibroblast growth factor 23 levels peaked 3 h after LPS treatment. Western blotting, immunostaining, and quantitative real-time PCR showed that LPS administration significantly decreased Npt2a protein expression in the brush border membrane (BBM) 3 h after injection, but there was no change in renal Npt2a mRNA levels. Moreover, tumor necrosis factor- injection also increased plasma iPTH and decreased renal BBM Npt2a expression. Importantly, we revealed that parathyroidectomized rats had impaired renal Pi excretion and BBM Npt2a expression in response to LPS. These results suggest that the downregulation of Npt2a expression in renal BBM through induction of plasma iPTH levels alter Pi homeostasis during LPS-induced acute inflammation.
(キーワード): Acute Disease / Animals / Calcium / Disease Models, Animal / Down-Regulation / Fibroblast Growth Factors / Inflammation / Injections, Intraperitoneal / Kidney / Lipopolysaccharides / Male / Mice / Mice, Inbred C3H / Mice, Inbred C57BL / Microvilli / Parathyroid Hormone / Parathyroidectomy / Phosphates / RNA, Messenger / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Time Factors / Tumor Necrosis Factor-alpha / Vitamin D
(徳島大学機関リポジトリ): ● Metadata: 106168
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00474.2013
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24500689; ● Search Scopus @ Elsevier (PMID): 24500689; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00474.2013

(徳島大学機関リポジトリ: 106168, DOI: 10.1152/ajprenal.00474.2013, PubMed: 24500689) Ritsuko Ohnishi, Hiroko Segawa, Tomoyo Ohmoto, Shohei Sasaki, Ai Hanazaki, Ayaka Mori, Kayo Ikuta, Junya Furutani, Eri Kawakami, Sawako Tatsumi, Yasuhiro Hamada and Ken-ichi Miyamoto :
Effect of dietary components on renal inorganic phosphate (Pi) excretion induced by a Pi-depleted diet.,
The Journal of Medical Investigation : JMI, Vol.61, No.1-2, 162-170, 2014.

(要約): Dietary inorganic phosphate (Pi) is the most important factor in the regulation of renal Pi excretion. Recent studies suggest the presence of an enteric-renal signaling axis for dietary Pi as well as the existence of a mechanism by which the intestine detects changes in luminal Pi concentrations. The mechanisms of intestinal Pi sensing, however, are unknown. In the present study, we focused on Pi depletion signals and investigated the effects of dietary components on intestinal Pi sensing. After feeding rats experimental diets for 3 days, we investigated urinary Pi excretion and plasma biochemical parameters. Renal Pi excretion was suppressed in rats fed a low-Pi diet (0.02% Pi). Elimination of dietary calcium (Ca) completely blocked the suppression of Pi excretion, suggesting that the presence of Ca is essential for the Pi depletion signal. Furthermore, a minimum Ca content of more than 0.02% was necessary for the Pi depletion signal. Magnesium, lanthanum, and strontium, which are agonists of calcium sensing receptor, instead of Ca, reduced Pi excretion. Therefore, dietary Ca appears to be important for the Pi depletion-sensing mechanism in the gastrointestinal tract. In addition, the calcium sensing receptor may be involved in the Pi depletion signal.
(キーワード): dietary phosphate / sensing / calcium / phosphate excretion
(徳島大学機関リポジトリ): ● Metadata: 109545
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.61.162
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705762; ● CiNii @ 国立情報学研究所 (CRID): 1390001204244658176; ● Summary page in Scopus @ Elsevier: 2-s2.0-84897932982

(徳島大学機関リポジトリ: 109545, DOI: 10.2152/jmi.61.162, PubMed: 24705762, CiNii: 1390001204244658176, Elsevier: Scopus) Rika Kuriwaka-Kido, Shinsuke Kido, Yuka Miyatani, Yuji Ito, Takeshi Kondo, Takashi Omatsu, Bingzi Dong, Itsuro Endo, Ken-ichi Miyamoto and Toshio Matsumoto :
Parathyroid hormone (1-34) counteracts the suppression of interleukin-11 expression by glucocorticoid in murine osteoblasts: a possible mechanism for stimulating osteoblast differentiation against glucocorticoid excess.,
Endocrinology, Vol.154, No.3, 1156-1167, 2013.

(要約): Glucocorticoid (GC) excess causes a rapid loss of bone with a reduction in bone formation. Intermittent PTH (1-34) administration stimulates bone formation and counteracts the inhibition of bone formation by GC excess. We have previously demonstrated that mechanical strain enhances interleukin (IL)-11 gene transcription by a rapid induction of FosB expression and protein kinase C (PKC)--mediated phosphorylation of phosphorylated mothers against decapentaplegic (Smad)-1. Because IL-11 suppresses the expression of dickkopf-1 and -2 and stimulates Wnt signaling, IL-11 appears to mediate at least a part of the effect of mechanical strain on osteoblast differentiation and bone formation. The present study was undertaken to examine the effect of PTH(1-34) and GCs on IL-11 expression in murine primary osteoblasts (mPOBs). PTH(1-34) treatment of mPOBs enhanced IL-11 expression in a time- and dose-dependent manner. PTH(1-34) also stimulated FosB expression and Smad1 phosphorylation, which cooperatively stimulated IL-11 gene transcription. PTH(1-34)-induced Smad1 phosphorylation was mediated via PKC and was abrogated in mPOBs from PKC knockout mice. Dexamethasone suppressed IL-11 gene transcription enhanced by PTH(1-34) without affecting FosB expression or Smad1 phosphorylation, and dexamethasone-GC receptor complex was bound to JunD, which forms heterodimers with FosB. High doses of PTH(1-34) counteracted the effect of dexamethasone on apoptosis of mPOBs, which was blunted by neutralizing anti-IL-11 antibody or IL-11 small interfering RNA. These results demonstrate that PTH(1-34) and GCs interact to regulate IL-11 expression in parallel with osteoblast differentiation and apoptosis and suggest that PTH(1-34) and dexamethasone may regulate osteoblast differentiation and apoptosis via their effect on IL-11 expression.
(キーワード): Alkaline Phosphatase / Animals / Apoptosis / Cell Differentiation / Cells, Cultured / Dexamethasone / Gene Expression Regulation / Interleukin-11 / Mice / Osteoblasts / Osteocalcin / Osteoprotegerin / Parathyroid Hormone / Phosphorylation / Promoter Regions, Genetic / Protein Kinase C-delta / Proto-Oncogene Proteins c-fos / Proto-Oncogene Proteins c-jun / RANK Ligand / RNA, Messenger / RNA, Small Interfering / Receptors, Glucocorticoid / Signal Transduction / Smad1 Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1210/en.2013-1915
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23397032; ● Search Scopus @ Elsevier (PMID): 23397032; ● Search Scopus @ Elsevier (DOI): 10.1210/en.2013-1915

(DOI: 10.1210/en.2013-1915, PubMed: 23397032) Sarasa Tanaka, Hironori Yamamoto, Otoki Nakahashi, Mariko Ishiguro, Yuichiro Takei, Masashi Masuda, Mina Kozai, Shoko Ikeda, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
Hypercholesterolemia and effects of high cholesterol diet in type IIa sodium-dependent phosphate co-transporter (Npt2a) deficient mice.,
The Journal of Medical Investigation : JMI, Vol.60, No.3-4, 191-196, 2013.

(要約): The type IIa sodium-dependent phosphate co-transporter (Npt2a) is important to maintain renal inorganic phosphate (Pi) homeostasis and the plasma Pi levels. It has reported that disorder of Pi metabolism in kidney can be risk factors for cardiovascular disease as well as hypercholesterolemia. However, the relationship between Pi and cholesterol metabolism has not been clarified. The current study investigated the effects of Npt2a gene ablation that is known as hypophosphatemia model on cholesterol metabolism in mice. Npt2a deficient (Npt2a(-/-)) mice and wild type mice were fed diets with or without 2% cholesterol for 12 days. Plasma lipid and lipoprotein profile analysis revealed that plasma lipid levels (total, LDL and HDL cholesterol) were significantly higher in Npt2a(-/-) mice than wild type (WT) mice. Interestingly, high cholesterol diet markedly increased plasma levels of total, LDL and HDL cholesterol in WT mice, but not Npt2a(-/-) mice. On the other hand, there were no differences in body and liver weight, intake and hepatic lipid accumulation between WT and Npt2a(-/-) mice. These results suggest that ablation of Npt2a gene induces hypercholesterolemia and affects the ability to respond normally to dietary cholesterol.
(キーワード): Animals / コレステロール (cholesterol) / Cholesterol, Dietary / Female / Hypercholesterolemia / Lipids / Liver / Male / Mice / ノックアウトマウス (knockout mice) / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa
(徳島大学機関リポジトリ): ● Metadata: 106356
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.60.191
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24190035; ● Summary page in Scopus @ Elsevier: 2-s2.0-84887001043

(徳島大学機関リポジトリ: 106356, DOI: 10.2152/jmi.60.191, PubMed: 24190035, Elsevier: Scopus) 木戸慎介, 桑原頌治, 野村憲吾, 大井彰子, 辰巳佐和子, 瀬川博子, 宮本賢一 :
FGF23の作用と作用機序.,
25-31, 2012年. Shoji Kuwahara, Fumito Aranami, Hiroko Segawa, Akemi Onitsuka, Naoko Honda, Rieko Tominaga, Etsuyo Hanabusa, Ichiro Kaneko, Setsuko Yamanaka, Shohei Sasaki, Akiko Ohi, Kengo Nomura, Sawako Tatsumi, Shinsuke Kido, Mikiko Ito and Ken-ichi Miyamoto :
Identification and functional analysis of a splice variant of mouse sodium-dependent phosphate transporter Npt2c.,
The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 116-126, 2012.

(要約): Mutations in the SLC34A3 gene, a sodium-dependent inorganic phosphate (Pi) cotransporter, also referred to as NaPi IIc, causes hereditary hypophosphatemic rickets with hypercalciuria (HHRH), an autosomal recessive disorder. In human and rodent, NaPi IIc is mainly localized in the apical membrane of renal proximal tubular cells. In this study, we identified mouse NaPi IIc variant (Npt2c-v1) that lacks the part of the exon 3 sequence that includes the assumed translation initiation site of Npt2c. Microinjection of mouse Npt2c-v1 cRNA into Xenopus oocytes demonstrated that Npt2c-v1 showed sodium-dependent Pi cotransport activity. The characterization of pH dependency showed activation at extracellular alkaline-pH. Furthermore, Npt2c-v1 mediated Pi transport activity was significantly higher at any pH value than those of Npt2c. In an in vitro study, the localization of the Npt2c-v1 protein was detected in the apical membrane in opossum kidney cells. The expression of Npt2c-v1 mRNA was detected in the heart, spleen, testis, uterus, placenta, femur, cerebellum, hippocampus, diencephalon and brain stem of mouse. Using mouse bone primary cultured cells, we showed the expression of Npt2c-v1 mRNA. In addition, the Npt2c protein was detected in the spermatozoa head. Thus, Npt2c-v1 was expressed in extra-renal tissues such as epididymal spermatozoa and may function as a sodium-dependent phosphate transporter.
(キーワード): Alternative Splicing / Animals / COS Cells / Cercopithecus aethiops / Female / Kidney / Male / Mice / Mice, Inbred C57BL / Opossums / Osteoblasts / Osteocytes / Primary Cell Culture / Sodium-Phosphate Cotransporter Proteins, Type IIc
(徳島大学機関リポジトリ): ● Metadata: 106008
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.59.116
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22450000; ● Search Scopus @ Elsevier (PMID): 22450000; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.116

(徳島大学機関リポジトリ: 106008, DOI: 10.2152/jmi.59.116, PubMed: 22450000) Sakiko Haito-Sugino, Mikiko Ito, Akiko Ohi, Yuji Shiozaki, Natsumi Kangawa, Takashi Nishiyama, Fumito Aranami, Shohei Sasaki, Ayaka Mori, Shinsuke Kido, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto :
Processing and stability of type IIc sodium-dependent phosphate cotransporter mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria.,
American Journal of Physiology, Cell Physiology, Vol.302, No.9, C1316-30, 2011.

(要約): Mutations in the apically located Na(+)-dependent phosphate (NaPi) cotransporter, SLC34A3 (NaPi-IIc), are a cause of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We have characterized the impact of several HHRH mutations on the processing and stability of human NaPi-IIc. Mutations S138F, G196R, R468W, R564C, and c.228delC in human NaPi-IIc significantly decreased the levels of NaPi cotransport activities in Xenopus oocytes. In S138F and R564C mutant proteins, this reduction is a result of a decrease in the V(max) for P(i), but not the K(m). G196R, R468W, and c.228delC mutants were not localized to oocyte membranes. In opossum kidney (OK) cells, cell surface labeling, microscopic confocal imaging, and pulse-chase experiments showed that G196R and R468W mutations resulted in an absence of cell surface expression owing to endoplasmic reticulum (ER) retention. G196R and R468W mutants could be partially stabilized by low temperature. In blue native-polyacrylamide gel electrophoresis analysis, G196R and R468W mutants were either denatured or present in an aggregation complex. In contrast, S138F and R564C mutants were trafficked to the cell surface, but more rapidly degraded than WT protein. The c.228delC mutant did not affect endogenous NaPi uptake in OK cells. Thus, G196R and R468W mutations cause ER retention, while S138F and R564C mutations stimulate degradation of human NaPi-IIc in renal epithelial cells. Together, these data suggest that the NaPi-IIc mutants in HHRH show defective processing and stability.
(キーワード): Animals / Blotting, Western / Humans / Hypercalciuria / Hypophosphatemic Rickets, X-Linked Dominant / Immunoprecipitation / Microscopy, Confocal / Mutagenesis, Site-Directed / Mutation / Polymerase Chain Reaction / Protein Stability / Sodium-Phosphate Cotransporter Proteins, Type IIc / Transfection / Xenopus laevis
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpcell.00314.2011
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22159077; ● Search Scopus @ Elsevier (PMID): 22159077; ● Search Scopus @ Elsevier (DOI): 10.1152/ajpcell.00314.2011

(DOI: 10.1152/ajpcell.00314.2011, PubMed: 22159077) Akiko Ohi, Kengo Nomura and Ken-ichi Miyamoto :
[Calcium pros and cons significance and risk of phosphorus supplementation. The risk of dietary phosphorus intake].,
Clinical Calcium, Vol.21, No.12, 171-174, 2011.

(要約): Dietary intake of phosphorus (Pi) is an important determinant of Pi balance in patients who have chronic kidney disease (CKD) and a reduced GFR. High dietary Pi burden may promote vascular calcification and cardiovascular events. Recently, Ohnishi and Razzaque suggest that phosphate toxicity accelerates the mammalian aging process and that reducing the phosphate burden can delay the aging (FASEB J 24, 3562, 2010) . Dietary Pi is derived largely from foods with high protein content or food additives. Accurate information on the Pi content of foods is needed to achieve a low Pi intake and effectively manage CKD and the aging. In this review, we discuss the risk of dietary Pi intake in CKD and the aging.
(キーワード): Aging / Cardiovascular Diseases / Chronic Disease / Food Analysis / Glomerular Filtration Rate / Humans / Kidney Diseases / Phosphorus / Phosphorus, Dietary / Risk / Vascular Calcification
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22133837; ● Summary page in Scopus @ Elsevier: 2-s2.0-84857067805

(PubMed: 22133837, Elsevier: Scopus) Akiko Ohi, Etsuyo Hanabusa, Otoya Ueda, Hiroko Segawa, Naoshi Horiba, Ichiro Kaneko, Shoji Kuwahara, Tomo Mukai, Shohei Sasaki, Rieko Tominaga, Junya Furutani, Fumito Aranami, Shuichi Ohtomo, Yumiko Oikawa, Yousuke Kawase, A Naoko Wada, Takanori Tachibe, Mami Kakefuda, Hiromi Tateishi, Kaoru Matsumoto, Sawako Tatsumi, Shinsuke Kido, Naoshi Fukushima, Kou-Ichi Jishage and Ken-ichi Miyamoto :
Inorganic phosphate homeostasis in sodium-dependent phosphate cotransporter Npt2b^+/- mice.,
American Journal of Physiology, Renal Physiology, Vol.301, No.5, F1105-13, 2011.

(要約): An inorganic phosphate (P(i))-restricted diet is important for patients with chronic kidney disease and patients on hemodialysis. Phosphate binders are essential for preventing hyperphosphatemia and ectopic calcification. The sodium-dependent P(i) (Na/P(i)) transport system is involved in intestinal P(i) absorption and is regulated by several factors. The type II sodium-dependent P(i) transporter Npt2b is expressed in the brush-border membrane in intestinal epithelial cells and transports P(i). In the present study, we analyzed the phenotype of Npt2b(-/-) and hetero(+/-) mice. Npt2b(-/-) mice died in utero soon after implantation, indicating that Npt2b is essential for early embryonic development. At 4 wk of age, Npt2b(+/-) mice showed hypophosphatemia and low urinary P(i) excretion. Plasma fibroblast growth factor 23 levels were significantly decreased and 1,25(OH)(2)D(3) levels were significantly increased in Npt2b(+/-) mice compared with Npt2b(+/+) mice. Npt2b mRNA levels were reduced to 50% that in Npt2b(+/+) mice. In contrast, renal Npt2a and Npt2c transporter protein levels were significantly increased in Npt2b(+/-) mice. At 20 wk of age, Npt2b(+/-) mice showed hypophosphaturia and reduced Na/P(i) cotransport activity in the distal intestine. Npt2b(+/+) mice with adenine-induced renal failure had hyperphosphatemia and high plasma creatinine levels. Npt2b(+/-) mice treated with adenine had significantly reduced plasma P(i) levels compared with Npt2b(+/+) mice. Intestinal Npt2b protein and Na(+)/P(i) transport activity levels were significantly lower in Npt2b(+/-) mice than in the Npt2b(+/+) mice. The findings of the present studies suggest that Npt2b is an important target for the prevention of hyperphosphatemia.
(キーワード): Adenine / Animals / Blotting, Western / Body Weight / Chromosomes, Artificial, Bacterial / DNA / Diet / Female / Genetic Vectors / Genotype / Homeostasis / Intestines / Mice / Mice, Inbred C57BL / Mice, Knockout / Microvilli / Phosphates / Polymerase Chain Reaction / Pregnancy / Renal Insufficiency / Sodium / Sodium-Phosphate Cotransporter Proteins, Type IIb
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00663.2010
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21816756; ● Search Scopus @ Elsevier (PMID): 21816756; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00663.2010

(DOI: 10.1152/ajprenal.00663.2010, PubMed: 21816756) Masafumi Fukagawa, Hirotaka Komaba and Ken-ichi Miyamoto :
Source matters: from phosphorus load to bioavailability.,
Clinical Journal of the American Society of Nephrology : CJASN, Vol.6, No.2, 239-240, 2011.

(キーワード): Biological Availability / Biological Markers / Chronic Disease / Diet, Vegetarian / Dietary Proteins / Fibroblast Growth Factors / Glomerular Filtration Rate / ホメオスタシス (homeostasis) / Humans / Kidney Diseases / Meat / Phosphorus, Dietary / Plant Proteins / Time Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.2215/CJN.11051210
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21292849; ● Search Scopus @ Elsevier (PMID): 21292849; ● Search Scopus @ Elsevier (DOI): 10.2215/CJN.11051210

(DOI: 10.2215/CJN.11051210, PubMed: 21292849) Ayako Tanimura, Fumiyo Yamada, Akihito Saito, Mikiko Ito, Toru Kimura, Naohiko Anzai, Daisuke Horie, Hironori Yamamoto, Ken-ichi Miyamoto, Yutaka Taketani and Eiji Takeda :
Analysis of different complexes of type IIa sodium-dependent phosphate transporter in rat renal cortex using blue-native polyacrylamide gel electrophoresis.,
The Journal of Medical Investigation : JMI, Vol.58, No.1-2, 140-147, 2011.

(要約): Type IIa sodium-dependent phosphate transporter (NaPi-IIa) can be localized in the apical plasma membrane of renal proximal tubule to carry out a rate-limiting step of phosphate reabsorption. For the apical localization, NaPi-IIa is required to form a macromolecular complex with some adaptor proteins such as Na(+)/H(+) exchanger regulatory factor 1 (NHERF-1) and ezrin. However, the detail of macromolecular complex containing NaPi-IIa in the apical membrane of the renal proximal tubular cells has not been clarified. In this study, we identified at least four different complexes (220, 480, 920, 1,100 kDa) containing NaPi-IIa by using blue-native polyacrylamide gel electrophoresis. Interestingly, LC-MS/MS analysis and immunoprecipitation analysis reveal that megalin is a component of larger complexes (920 and 1,100 kDa). In addition, NaPi-IIa can be heterogeneously co-localized with ezrin and megalin on the apical membrane of renal proximal tubuler cells by fluorescence microscopy analysis. These results suggest that NaPi-IIa can form some different complexes on the apical plasma membrane of renal proximal tubular cells.
(キーワード): Animals / Cell Line / Electrophoresis, Gel, Two-Dimensional / Electrophoresis, Polyacrylamide Gel / Kidney Cortex / Kidney Tubules, Proximal / LDL-Receptor Related Protein 2 / Male / Membrane Microdomains / 分子量 (molecular weight) / Multiprotein Complexes / Opossums / Protein Interaction Domains and Motifs / Rats / Rats, Sprague-Dawley / Sodium-Phosphate Cotransporter Proteins, Type IIa / Tandem Mass Spectrometry
(徳島大学機関リポジトリ): ● Metadata: 82750
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.58.140
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372499; ● Search Scopus @ Elsevier (PMID): 21372499; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.140

(徳島大学機関リポジトリ: 82750, DOI: 10.2152/jmi.58.140, PubMed: 21372499) Yuka Tomoe, Hiroko Segawa, Kazuyo Shiozawa, Ichiro Kaneko, Rieko Tominaga, Etsuyo Hanabusa, Fumito Aranami, Junya Furutani, Shoji Kuwahara, Sawako Tatsumi, Mitsuru Matsumoto, Mikiko Ito and Ken-ichi Miyamoto :
Phosphaturic action of fibroblast growth factor 23 in Npt2 null mice,
American Journal of Physiology, Renal Physiology, Vol.298, No.6, F1341-F1350, 2010.

(要約): In the present study, we evaluated the roles of type II and type III sodium-dependent P(i) cotransporters in fibroblast growth factor 23 (FGF23) activity by administering a vector encoding FGF23 with the R179Q mutation (FGF23M) to wild-type (WT) mice, Npt2a knockout (KO) mice, Npt2c KO mice, and Npt2a(-/-)Npt2c(-/-) mice (DKO mice). In Npt2a KO mice, FGF23M induced severe hypophosphatemia and markedly decreased the levels of Npt2c, type III Na-dependent P(i) transporter (PiT2) protein, and renal Na/P(i) transport activity. In contrast, in Npt2c KO mice, FGF23M decreased plasma phosphate levels comparable to those in FGF23M-injected WT mice. In DKO mice with severe hypophosphatemia, FGF23M administration did not induce an additional increase in urinary phosphate excretion. FGF23 administration significantly decreased intestinal Npt2b protein levels in WT mice but had no effect in Npt2a, Npt2c, and DKO mice, despite marked suppression of plasma 1,25(OH)(2)D(3) levels in all the mutant mice. The main findings were as follow: 1) FGF23-dependent phosphaturic activity in Npt2a KO mice is dependent on renal Npt2c and PiT-2 protein; 2) in DKO mice, renal P(i) reabsorption is not further decreased by FGF23M, but renal vitamin D synthesis is suppressed; and 3) downregulation of intestinal Npt2b may be mediated by a factor(s) other than 1,25(OH)(2)D(3). These findings suggest that Npt2a, Npt2c, and PiT-2 are necessary for the phosphaturic activity of FGF23. Thus complementary regulation of Npt2 family proteins may be involved in systemic P(i) homeostasis.
(キーワード): Animals / Calcitriol / カルシウム (calcium) / Fibroblast Growth Factors / Gene Transfer Techniques / Humans / 低リン血症 (hypophosphatemia) / Hypophosphatemia, Familial / Injections, Intravenous / Mice / Mice, Inbred C57BL / Mice, Knockout / Mutation / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type III / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIb / Sodium-Phosphate Cotransporter Proteins, Type IIc
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00375.2009
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20357029; ● Search Scopus @ Elsevier (PMID): 20357029; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00375.2009

(DOI: 10.1152/ajprenal.00375.2009, PubMed: 20357029) Mariko Ishiguro, Hironori Yamamoto, Masashi Masuda, Mina Kozai, Yuichiro Takei, Sarasa Tanaka, Tadatoshi Sato, Hiroko Segawa, Yutaka Taketani, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda :
Thyroid hormones regulate phosphate homoeostasis through transcriptional control of the renal type IIa sodium-dependent phosphate co-transporter (Npt2a) gene.,
The Biochemical Journal, Vol.427, No.1, 161-169, 2010.

(要約): The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. It has been demonstrated previously that renal Npt2a protein and its mRNA expression are both up-regulated by the thyroid hormone T3 (3,3',5-tri-iodothyronine) in rats. However, it has never been established whether the induction was mediated by a direct effect of thyroid hormones on the Npt2a promoter. To address the role of Npt2a in T3-dependent regulation of phosphate homoeostasis and to identify the molecular mechanisms by which thyroid hormones modulate Npt2a gene expression, mice were rendered pharmacologically hypo- and hyper-thyroid. Hypothyroid mice showed low levels of serum phosphate and a marked decrease in renal Npt2a protein abundance. Importantly, we also showed that Npt2a-deficient mice had impaired serum phosphate responsiveness to T3 compared with wild-type mice. Promoter analysis with a luciferase assay revealed that the transcriptional activity of a reporter gene containing the Npt2a promoter and intron 1 was dependent upon TRs (thyroid hormone receptors) and specifically increased by T3 in renal cells. Deletion analysis and EMSAs (electrophoretic mobility-shift assays) determined that there were unique TREs (thyroid-hormone-responsive elements) within intron 1 of the Npt2a gene. These results suggest that Npt2a plays a critical role as a T3-target gene, to control phosphate homoeostasis, and that T3 transcriptionally activates the Npt2a gene via TRs in a renal cell-specific manner.
(キーワード): Animals / COS Cells / Cercopithecus aethiops / Dogs / Electrophoretic Mobility Shift Assay / Female / Gene Expression Regulation / Hela Cells / 生体恒常性 (homeostasis) / Humans / Kidney / Luciferases / Male / Mice / Mice, Knockout / Phosphates / Promoter Regions, Genetic / Rats / Receptors, Thyroid Hormone / Response Elements / Sodium-Phosphate Cotransporter Proteins, Type IIa / Transcription, Genetic / Transcriptional Activation / Triiodothyronine
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/BJ20090671
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20088828; ● Summary page in Scopus @ Elsevier: 2-s2.0-77950874525

(DOI: 10.1042/BJ20090671, PubMed: 20088828, Elsevier: Scopus) Naoki Sawada, Yutaka Taketani, Norio Amizuka, Masako Ichikawa, Chiharu Ogawa, Kaori Nomoto, Kunitaka Nashiki, Tadatoshi Sato, Hidekazu Arai, Masashi Isshiki, Hiroko Segawa, Hironori Yamamoto, Ken-ichi Miyamoto and Eiji Takeda :
Caveolin-1 in extracellular matrix vesicles secreted from osteoblasts.,
Bone, Vol.41, No.1, 52-58, 2007.

(要約): Caveolin-1 is an essential and signature protein of caveolae, which are small invaginations of the plasma membrane enriched in cholesterol and sphingolipids. Although high levels of expression of caveolin-1 have been demonstrated in osteoblasts as well as endothelial cells, fibroblasts, and muscular cells, the role of caveolin-1 in osteoblasts has not been clarified. Here, we show that caveolin-1 is secreted from osteoblasts in the form of matrix vesicles; extracellular vesicles released from the plasma membrane of osteoblasts. In this study, caveolae and matrix vesicles were similarly enriched in cholesterol and sphingomyelin in fractions isolated from mineralizing MC3T3-E1 cells. Interestingly, in the MC3T3-E1 cells caveolin-1 was enriched in the matrix vesicle fraction as well as the caveolar membrane fraction, and the amount of caveolin-1 in the matrix vesicle fraction increased as differentiation progressed. Localization of caveolin-1 in matrix vesicles was also confirmed in murine tibia. Furthermore, overexpression of caveolin-1 enhanced matrix calcification in MC3T3-E1 cells, whereas knockdown of caveolin-1 diminished it. These results suggest that secreted caveolin-1 as a component of matrix vesicles may play an important role in osteoblast calcification.
(キーワード): 3T3 Cells / Alkaline Phosphatase / Animals / Base Sequence / Calcification, Physiologic / Caveolin 1 / Cell Differentiation / Cholesterol / DNA Primers / Extracellular Matrix / Gene Expression / Mice / Microscopy, Immunoelectron / Osteoblasts / Phosphates / RNA Interference / Secretory Vesicles / Sphingomyelins / Tibia
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bone.2007.02.030
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17448744; ● Search Scopus @ Elsevier (PMID): 17448744; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bone.2007.02.030

(DOI: 10.1016/j.bone.2007.02.030, PubMed: 17448744) Kazuyoshi Kitaoka, Atsushi Hattori, Sachiko Chikahisa, Ken-ichi Miyamoto, Yutaka Nakaya and Hiroyoshi Sei :
Vitamin A deficiency induces a decrease in EEG delta power during sleep in mice,
Brain Research, Vol.1150, 121-130, 2007.

(要約): Recent report (Maret, S., Franken, P., Dauvilliers, Y., Ghyselinck, N.B., Chambon, P., Tafti, M., 2005. Retinoic acid signaling affects cortical synchrony during sleep. Science 310, 111-113.) has suggested that vitamin A (retinol and its derivatives) is genetically involved in the electroencephalogram (EEG) delta oscillation during sleep. However, this finding has not yet been confirmed by other studies. In this study, we attempted to record the sleep EEG and behavior, and to quantify striatal monoamines in mice fed a vitamin A-deficient (VAD) diet for 4 weeks, in order to clarify the linkage between the delta oscillation and vitamin A. VAD mice demonstrated a significant decrease in the delta power of the EEG. However, 6-h sleep deprivation caused the recovery of the delta power in VAD mice to a level similar to that of the control. VAD also caused the decrease of spontaneous activity throughout 24-h period. Furthermore, dihydroxyphenylacetic acid, a metabolite of dopamine, was decreased significantly in the striatal tissue of VAD mice. Our present results suggest that the deficiency of vitamin A causes the attenuation of delta power in NREM sleep and spontaneous activity. These attenuations may be related to the alteration of striatal dopaminergic function.
(キーワード): 3,4-Dihydroxyphenylacetic Acid / Analysis of Variance / Animals / Behavior, Animal / Body Weight / Corpus Striatum / Delta Rhythm / Dopamine / Exploratory Behavior / Male / Mice / Mice, Inbred C57BL / Motor Activity / Serotonin / Sleep / Sleep Deprivation / Spectrum Analysis / Vitamin A / Vitamin A Deficiency
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.brainres.2007.02.077
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17400199; ● Search Scopus @ Elsevier (PMID): 17400199; ● Search Scopus @ Elsevier (DOI): 10.1016/j.brainres.2007.02.077

(DOI: 10.1016/j.brainres.2007.02.077, PubMed: 17400199) Sachiko Chikahisa, Atsuko Sano, Kazuyoshi Kitaoka, Ken-ichi Miyamoto and Hiroyoshi Sei :
Anxiolytic effect of music depends on ovarian steroid in female mice.,
Behavioural Brain Research, Vol.179, No.1, 50-59, 2007.

(要約): Music is known to be able to elicit emotional changes, including anxiolytic effects. The gonadal steroid hormones estradiol and progesterone have also been reported to play important roles in the modulation of anxiety. In the present study, we examined whether the effect of music on anxiety is related to ovarian steroid in female mice. Behavioral paradigms measuring anxiety were tested in gonadally intact (SHAM) and ovariectomized (OVX) female mice chronically treated with either placebo (OVX/Placebo), 17β-estradiol (OVX/E), or progesterone (OVX/P). In the elevated plus maze, light-dark transition, and marble burying tests, SHAM and OVX/P mice exposed to music showed less anxiety than those exposed to white noise or silence while OVX/placebo mice did not show these effects at all. OVX/E mice showed the anxiolytic effect of music only in the marble burying test. Furthermore, pretreatment with progesterone's metabolite inhibitor completely prevented the anxiolytic effect of music in behavioral tests, while pretreatment with a progesterone receptor blocker did not prevent the anxiolytic effect of music. These results suggest that exposure to music reduces anxiety levels, and ovarian steroids, mainly progesterone, may be involved in the anxiolytic effect of music observed in female mice.
(キーワード): Anxiety / Music / 17β-estradio / Progesterone / Female mice
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbr.2007.01.010
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17280725; ● Search Scopus @ Elsevier (PMID): 17280725; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbr.2007.01.010

(DOI: 10.1016/j.bbr.2007.01.010, PubMed: 17280725) Masashi Kuwahata, Y Tomoe, Nagakatsu Harada, S Amano, Hiroko Segawa, S Tatsumi, Mikiko Ito, T Oka and Ken-ichi Miyamoto :
Characterization of the molecular mechanisms involved in the increased insulin secretion in rats with acute liver failure.,
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1772, No.1, 60-65, 2007.

(要約): To investigate the mechanism of hyperinsulinaemia in rats with acute liver failure induced by the administration of d-galactosamine (GalN), we focused on the role of polyprimidine tract-binding protein (PTB) in islet insulin synthesis. Recent reports indicate that PTB binds and stabilizes mRNA encoding insulin and insulin secretory granule proteins, including islet cell autoantigen 512 (ICA512), prohormone convertase 1/3 (PC1/3), and PC2. In the present study, glucose-stimulated insulin secretion was significantly increased in GalN-treated rats compared to controls. Levels of mRNA encoding insulin 1, ICA512, and PC1/3 were increased in the pancreatic islets of GalN-treated rats. This mRNA level elevation was not prevented by pretreatment with actinomycin D. When the PTB-binding site in insulin 1 mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from GalN-treated rats compared to the level in control rats. The cytosolic fraction obtained from pancreatic islets obtained from GalN-treated rats had an increased PTB level compared to the levels obtained from the pancreatic islets of control rats. These findings suggest that, in rats with acute liver failure, cytosolic PTB binds and stabilizes mRNA encoding insulin and its secretory granule proteins.
(キーワード): Alanine Transaminase / Animals / Blood Glucose / Disease Models, Animal / Galactosamine / Hyperinsulinism / Insulin / Islets of Langerhans / Liver Failure, Acute / Male / Organ Size / Polypyrimidine Tract-Binding Protein / RNA, Messenger / Rats / Rats, Sprague-Dawley / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbadis.2006.10.001
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17097861; ● Search Scopus @ Elsevier (PMID): 17097861; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2006.10.001

(DOI: 10.1016/j.bbadis.2006.10.001, PubMed: 17097861) Hiroko Segawa, Setsuko Yamanaka, Akemi Onitsuka, Yuka Tomoe, Masashi Kuwahata, Mikiko Ito, Yutaka Taketani and Ken-ichi Miyamoto :
Parathyroid hormone-dependent endocytosis of renal type IIc Na-Pi cotransporter.,
American Journal of Physiology, Renal Physiology, Vol.292, No.1, F395-F403, 2007.

(要約): Hereditary hypophosphatemic rickets with hypercalciuria results from mutations of the renal type IIc Na-P(i) cotransporter gene, suggesting that the type IIc transporter plays a prominent role in renal phosphate handling. The goal of the present study was to investigate the regulation of the type IIc Na-P(i) cotransporter by parathyroid hormone (PTH). Type IIc Na-P(i) cotransporter levels were markedly increased in thyroparathyroidectomized (TPTX) rats. Four hours after administration of PTH, type IIc transporter protein levels were markedly decreased in the apical membrane fraction but recovered to baseline levels at 24 h. Immunohistochemical analyses demonstrated the presence of the type IIc transporter in the apical membrane and subapical compartments in the proximal tubular cells in TPTX animals. After administration of PTH, the intensity of immunoreactive signals in apical and subapical type IIc transporter decreased in the renal proximal tubular cells in TPTX rats. Colchicine completely blocked the internalization of the type IIc transporter. In addition, leupeptin prevented the PTH-mediated degradation of the type IIa transporter in lysosomes but had no effect on PTH-mediated degradation of the lysosomal type IIc transporter. In PTH-treated TPTX rats, the internalization of the type IIc transporter occurred after administration of PTH(1-34) (PKA and PKC activator) or PTH(3-34) (PKC activator). Thus the present study demonstrated that PTH is a major hormonal regulator of the type IIc Na-P(i) cotransporter in renal proximal tubules.
(キーワード): Animals / Blotting, Northern / Cell Membrane / Endocytosis / Immunohistochemistry / Kidney / Lysosomes / Male / Microscopy, Fluorescence / Microtubules / Microvilli / Parathyroid Hormone / Parathyroidectomy / Peptide Fragments / Phosphates / RNA / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins, Type IIa / Thyroidectomy
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00100.2006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16985216; ● Search Scopus @ Elsevier (PMID): 16985216; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00100.2006

(DOI: 10.1152/ajprenal.00100.2006, PubMed: 16985216) 宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 :
リンとビタミンDの相互作用,
整形・災害外科, Vol.49, No.12, 1365-1370, 2006年.

(キーワード): Transporter / Kidney / FGF23
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520291855700655232

(CiNii: 1520291855700655232) Ken-ichi Miyamoto, Mikiko Ito, Hiroko Segawa and Masashi Kuwahata :
Molecular mechanism in biological transport in the kidney: Sodium-dependent glucose, phosphate, amino acid transporters.,
Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.64, 145-149, 2006.

(キーワード): Amino Acid Transport Systems, Neutral / Amino Acids, Neutral / Animals / Biological Transport / GABA Plasma Membrane Transport Proteins / Glucose / Humans / Kidney Tubules / Phosphates / Sodium-Glucose Transporter 1 / Sodium-Glucose Transporter 2 / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIc
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16523877; ● Search Scopus @ Elsevier (PMID): 16523877

(PubMed: 16523877) 宮本賢一, 瀬川博子 :
FGF23,
医学のあゆみ, Vol.216, No.2, 185-186, 2006年. 宮本賢一, 瀬川博子, 伊藤美紀子, 辰巳佐和子, 竹谷豊 :
栄養素の代謝と生理機能,
病態栄養専門師のための病態栄養ガイドブック, 14-19, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488265

(CiNii: 1020000781987488265) 伊藤美紀子, 拝藤紗貴子, 宮本賢一 :
リン制限は糖代謝を制御して寿命を延長させる,
食品工業, Vol.49, No.18, 44-51, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1521417754909593088

(CiNii: 1521417754909593088) 瀬川博子, 塩澤和代, 鬼塚朱美, 荒波史, 古谷順也, 伊藤美紀子, 桑波田雅士, 宮本賢一 :
リン酸トランスポーターをめぐる最近の話題,
腎と透析, Vol.61, No.1, 125-130, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1010282256960838282

(CiNii: 1010282256960838282) 宮本賢一, 伊藤美紀子 :
Neutral endopeptidase family of protein.,
腎と透析, Vol.60, No.4, 546-548, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1010282256960838281

(CiNii: 1010282256960838281) 宮本賢一, 伊藤美紀子, 瀬川博子, 桑波田雅士 :
ナトリウム・グルコース，ナトリウム・リン，ナトリウム・アミノ酸共役トランスポーター,
日本臨牀, Vol.64, No.2, 145-149, 2006年. 宮本賢一, 竹谷豊, 伊藤美紀子, 瀬川博子 :
ナトリウム依存症リントランスポータ-の調節機構,
Annual Review 腎臓, 216-220, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488258

(CiNii: 1020000781987488258) 瀬川博子, 宮本賢一 :
生体内におけるリンの役割, --- 光と影 ---,
腎と透析, Vol.60, No.1, 36-41, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488257

(CiNii: 1020000781987488257) Hironori Yamamoto, Yoshiko Tani, Kumi Kobayashi, Yutaka Taketani, Tadatoshi Sato, Hidekazu Arai, Kyoko Morita, Ken-ichi Miyamoto, John Wesley Pike, Shigeaki Kato and Eiji Takeda :
Alternative promoters and renal cell-specific regulation of the mouse type IIa sodium-dependent phosphate cotransporter gene,
Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Vol.1732, No.1-3, 43-52, 2005.

(要約): The type IIa sodium-dependent phosphate cotransporter (NPT2a) expressed in renal proximal tubules represents an important determinant in maintaining inorganic phosphate (Pi) homeostasis. In the present study, we identified two variant transcripts of the mouse NPT2a gene, Npt2a-v1 and Npt2a-v2, characterized by the presence of alternative first exons (either exon 1A or exon 1B). The chromosomal structure analysis revealed that the Npt2a gene comprises of two promoters (promoters 1 and 2) and 14 exons, and spans approximately 17 kb. Quantitative PCR analysis showed that renal mRNA levels of both the variants markedly decreased in X-linked vitamin D-resistant hypophosphatemic rickets (Hyp) mice compared to normal littermates. Interestingly, transcriptional activity of a reporter gene, containing Npt2a promoters 1 and 2, was renal cell-specifically increased by 1alpha, 25(OH)2D3 and its analogs. The deletion analysis revealed that the CAAT box in the Npt2a promoter 2 is important for the 1alpha, 25(OH)2D3-dependent renal cell-specific activation of the reporter gene. These data suggested that two alternative promoters control the renal expression of Npt2a gene and both Npt2a variant transcripts are down regulated in Hyp mice.
(キーワード): 5' Flanking Region / 5' Untranslated Regions / Animals / Base Sequence / COS Cells / Caco-2 Cells / Calcitriol / Cells, Cultured / Cercopithecus aethiops / Chromosomes, Mammalian / Exons / Gene Expression Regulation / Humans / Kidney / Mice / Mice, Inbred C57BL / Mice, Obese / Molecular Sequence Data / Opossums / Organ Specificity / Promoter Regions, Genetic / RNA, Messenger / Sequence Deletion / Sodium-Phosphate Cotransporter Proteins, Type IIa
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbaexp.2005.11.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16380173; ● Search Scopus @ Elsevier (PMID): 16380173; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbaexp.2005.11.003

(DOI: 10.1016/j.bbaexp.2005.11.003, PubMed: 16380173) Kunitaka Nashiki, Yutaka Taketani, Tomoko Takeichi, Naoki Sawada, Hironori Yamamoto, Masako Ichikawa, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda :
Role of membrane microdomains in PTH-mediated down-regulation of NaPi-IIa in opossum kidney cells,
Kidney International, Vol.68, No.3, 1137-1147, 2005.

(要約): Parathyroid hormone (PTH) rapidly down-regulates type IIa sodium-dependent phosphate transporter (NaPi-IIa) via an endocytic pathway. Since the relationship between PTH signaling and NaPi-IIa endocytosis has not been explored, we investigated the role of membrane microdomains in this process. We examined the submembrane localization of NaPi-IIa in opossum kidney (OK-N2) cells that stably expressed human NaPi-IIa, and searched for a PTH-induced specific phosphorylating substrate on their membrane microdomains by immunoblotting with specific antibody against phospho substrates of protein kinases. We found that NaPi-IIa was primarily localized in low-density membrane (LDM) domains of the plasma membrane; PTH reduced the levels of immunoreactive NaPi-IIa in these domains. Furthermore, PTH activated both protein kinase A (PKA) and protein kinase Calpha (PKCa) and increased the phosphorylation of 250 kD and 80 kD substrates; this latter substrate was identified as ezrin, which a member of the ezrin-radixin-moesin (ERM) protein family. In response to PTH, ezrin was phosphorylated by both PKA and PKC. Dominant negative ezrin blocked the reduction in NaPi-IIa expression in the LDM domains that was induced by PTH. These data suggest that NaPi-IIa and PTH-induced phosphorylated proteins that include ezrin are compartmentalized in LDM microdomains. This compartmentalization may play an important role in the down-regulation of NaPi-IIa via endocytosis.
(キーワード): Animals / Antineoplastic Agents / Cell Compartmentation / Cell Line / Chlorpromazine / Cyclic AMP-Dependent Protein Kinases / Cyclodextrins / Cytochalasin D / Cytoskeletal Proteins / Dopamine Antagonists / Down-Regulation / Endocytosis / Humans / Immunohistochemistry / Kidney / Nocodazole / Nucleic Acid Synthesis Inhibitors / Opossums / Parathyroid Hormone / Phosphates / Phosphoproteins / Phosphorylation / Protein Kinase C-alpha / Protein Structure, Tertiary / Sodium-Phosphate Cotransporter Proteins, Type IIa
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1523-1755.2005.00505.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16105044; ● Search Scopus @ Elsevier (PMID): 16105044; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1523-1755.2005.00505.x

(DOI: 10.1111/j.1523-1755.2005.00505.x, PubMed: 16105044) Yoshio Inoue, Hiroko Segawa, Ichiro Kaneko, Setsuko Yamanaka, Kenichiro Kusano, Eri Kawakami, Junya Furutani, Mikiko Ito, Masashi Kuwahata, Hitoshi Saito, Naoshi Fukushima, Shigeaki Kato, Hiro-omi Kanayama and Ken-ichi Miyamoto :
Role of the vitamin D receptor in FGF23 action on phosphate metabolism,
The Biochemical Journal, Vol.390, No.1, 325-331, 2005.

(要約): FGF23 (fibroblast growth factor 23) is a novel phosphaturic factor that influences vitamin D metabolism and renal re-absorption of Pi. The goal of the present study was to characterize the role of the VDR (vitamin D receptor) in FGF23 action using VDR(-/-) (VDR null) mice. Injection of FGF23M (naked DNA encoding the R179Q mutant of human FGF23) into VDR(-/-) and wildtype VDR(+/+) mice resulted in an elevation in serum FGF23 levels, but had no effect on serum calcium or parathyroid hormone levels. In contrast, injection of FGF23M resulted in significant decreases in serum Pi levels, renal Na/Pi co-transport activity and type II transporter protein levels in both groups when compared with controls injected with mock vector or with FGFWT (naked DNA encoding wild-type human FGF23). Injection of FGF23M resulted in a decrease in 25-hydroxyvitamin D 1a-hydroxylase mRNA levels in VDR(-/-) and VDR(+/+) mice, while 25-hydroxyvitamin D 24-hydroxylase mRNA levels were significantly increased in FGF23M-treated animals compared with mock vector control- or FGF23WT-treated animals. The degree of 24-hydroxylase induction by FGF23M was dependent on the VDR, since FGF23M significantly reduced the levels of serum 1,25(OH)2D3 [1,25-hydroxyvitamin D3] in VDR(+/+) mice, but not in VDR(-/-) mice. We conclude that FGF23 reduces renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that is independent of the VDR. In contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction of serum 1,25(OH)2D3 levels induced by FGF23 are dependent on the VDR.
(キーワード): fibroblast growth factor 23 / kidney / phosphate transport / vitamin D receptor
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/BJ20041799
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15885032; ● Search Scopus @ Elsevier (PMID): 15885032; ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20041799

(DOI: 10.1042/BJ20041799, PubMed: 15885032) Ken-ichi Miyamoto, Mikiko Ito, Masashi Kuwahata, Shigeaki Kato and Hiroko Segawa :
Inhibition of Intestinal Sodium-dependent Inorganic phosphate Transport by Fibroblast Growth Factor 23,
Therapeutic Apheresis and Dialysis, Vol.9, No.4, 331-335, 2005.

(要約): The mechanisms by which fibroblast growth factor 23 (FGF23) alters inorganic phosphate (Pi) homeostasis is not entirely clear. In the present study, we examined the effect of FGF23 on intestinal sodium-dependent Pi transport in mice. Injection of FGF23(R179Q) markedly reduced serum Pi and 1,25(OH)2D3 levels in normal mice. Those animals show the reduction of intestinal sodium-dependent Pi transport activity and the amount of type IIb sodium-dependent Pi cotransporter (type IIb NaPi) protein in the brush border membrane vesicles. In vitamin D receptor null mice (VDR-/-), FGF23(R179Q) had no effect on intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels. The present study suggests that FGF23(R179Q) reduces intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels by a mechanism that is dependent on VDR.
(キーワード): Fibroblast growth factor 23 / Inorganic phosphate / Small intestine / Vitamin D receptor
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1744-9987.2005.00292.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16076377; ● Search Scopus @ Elsevier (PMID): 16076377; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1744-9987.2005.00292.x

(DOI: 10.1111/j.1744-9987.2005.00292.x, PubMed: 16076377) Akira Matsuo, Tamotsu Negoro, Tomohisa Seo, Yuki Kitao, Masanori Shindo, Hiroko Segawa and Ken-ichi Miyamoto :
Inhibitory effect of JTP-59557, a new triazole derivative, on intestinal phosphate transport in vitro and in vivo,
European Journal of Pharmacology, Vol.517, No.1-2, 111-119, 2005.

(要約): JTP-59557 [(-)-4-(2-tert-Butyl-4,5-dichlorophenyl)-5-(5-trifluoromethylpyridin-2-ylsulfanyl)-4H-[1,2,4]triazol-3-ol] showed an inhibitory effect on Na(+)-dependent inorganic phosphate (Pi) transport in intestinal brush border membrane vesicles with an IC(50) value of 0.40 microM in rabbit and with an IC(50) of 0.19 microM in rat, without affecting Na(+)-independent Pi and Na(+)-dependent d-glucose transport activities. In Chinese hamster ovary (CHO) cells expressing human type IIb Na/Pi cotransporter (type IIb), JTP-59557 decreased human type IIb-mediated Pi uptake with an IC(50) of 0.12 microM. In rabbit intestinal brush border membrane vesicles, JTP-59557 behaved as a noncompetitive inhibitor with respect to Pi. In an in vivo study, single administration of JTP-59557 significantly decreased the intestinal Pi absorption rate, when either Pi solution or laboratory chow was given to rats. In this report, we show that JTP-59557 is a potent, selective, stereospecific, noncompetitive inhibitor of intestinal Na/Pi cotransporters including type IIb, and it may represent a new class of intestinal Pi absorption inhibitor.
(キーワード): JTP-59557 / Type 2b Na/Pi cotransporter / Intestinal Na+-dependent Pi transport / Pi absorption
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2005.05.003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15961073; ● Search Scopus @ Elsevier (PMID): 15961073; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2005.05.003

(DOI: 10.1016/j.ejphar.2005.05.003, PubMed: 15961073) Mikiko Ito, Yuko Sakai, Mari Furumoto, Hiroko Segawa, Sakiko Haito, Setsuko Yamanaka, Rie Nakamura, Masashi Kuwahata and Ken-ichi Miyamoto :
Vitamin D and phosphate regulate fibroblast growth factor-23 in K-562 cells,
American Journal of Physiology, Endocrinology and Metabolism, Vol.288, No.6, E1101-E1109, 2005.

(要約): Fibroblast growth factor-23 (FGF-23) has been recently identified as playing an important pathophysiological role in phosphate homeostasis and vitamin D metabolism. To elucidate the precise physiological regulation of FGF-23, we characterized the mouse FGF-23 5'-flanking region and analyzed its promoter activity. The 5'-flanking region of the mouse FGF-23 gene contained a TFIID site (TATA box) and several putative transcription factor binding sites, including MZF1, GATA-1 and c-Ets-1 motifs, but it did not contain the typical sequences of the vitamin D response element. Plasmids encoding 554-bp (pGL/-0.6), 364-bp (pGL/-0.4) and 200-bp (pGL/-0.13) promoter regions containing the TFIID element and +1-bp fragments drove the downstream expression of a luciferase reporter gene in transfection assays. We also found that FGF-23 mRNA was expressed in K-562 erythroleukemia cell lines but not in MC3T3-E1, Raji, or Hep G2 human carcinoma cells. Treatment with 1,25-dihydroxyvitamin D3 in the presence of high phosphate markedly stimulated pGL/-0.6 activity, but calcium had no effect. In addition, the plasma FGF-23 levels were affected by the dietary and plasma inorganic phosphate concentrations. Finally, the levels of plasma FGF-23 in vitamin D receptor-null mice were significantly lower than in wild-type mice. The presents study demonstrated that vitamin D and the plasma phosphate level are important regulators of the transcription of the mouse FGF-23 gene.
(キーワード): Animals / Base Sequence / Calcitriol / Cloning, Molecular / DNA / Fibroblast Growth Factors / Humans / K562 Cells / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Molecular Sequence Data / Phosphates / Polymerase Chain Reaction / Promoter Regions, Genetic / RNA, Messenger / Receptors, Calcitriol / Vitamin D Response Element
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpendo.00502.2004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15671080; ● Search Scopus @ Elsevier (PMID): 15671080; ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00502.2004

(DOI: 10.1152/ajpendo.00502.2004, PubMed: 15671080) Mikiko Ito, Naoko Matsuka, Michiyo Izuka, Sakiko Haito, Yuko Sakai, Rie Nakamura, Hiroko Segawa, Masashi Kuwahata, Hironori Yamamoto, Wesley J Pike and Ken-ichi Miyamoto :
Characterization of inorganic phosphate transport in osteoclast-like cells,
American Journal of Physiology, Cell Physiology, Vol.288, No.4, 921-931, 2005.

(要約): Osteoclasts possess inorganic phosphate (Pi) transport systems to take up external Pi during bone resorption. In the present study, we characterized Pi transport in mouse osteoclast-like cells that were obtained by differentiation of macrophage RAW264.7 cells with receptor activator of NF-kappaB ligand (RANKL). In undifferentiated RAW264.7 cells, Pi transport into the cells was Na+ dependent, but after treatment with RANKL, Na+-independent Pi transport was significantly increased. In addition, compared with neutral pH, the activity of the Na+-independent Pi transport system in the osteoclast-like cells was markedly enhanced at pH 5.5. The Na+-independent system consisted of two components with Km of 0.35 mM and 7.5 mM. The inhibitors of Pi transport, phosphonoformic acid, and arsenate substantially decreased Pi transport. The proton ionophores nigericin and carbonyl cyanide p-trifluoromethoxyphenylhydrazone as well as a K+ ionophore, valinomycin, significantly suppressed Pi transport activity. Analysis of BCECF fluorescence indicated that Pi transport in osteoclast-like cells is coupled to a proton transport system. In addition, elevation of extracellular K+ ion stimulated Pi transport, suggesting that membrane voltage is involved in the regulation of Pi transport activity. Finally, bone particles significantly increased Na+-independent Pi transport activity in osteoclast-like cells. Thus, osteoclast-like cells have a Pi transport system with characteristics that are different from those of other Na+-dependent Pi transporters. We conclude that stimulation of Pi transport at acidic pH is necessary for bone resorption or for production of the large amounts of energy necessary for acidification of the extracellular environment.
(キーワード): Na+-dependent phosphate cotransporter / RAW264.7 / phosphate uptake
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpcell.00412.2004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15601753; ● Search Scopus @ Elsevier (PMID): 15601753; ● Search Scopus @ Elsevier (DOI): 10.1152/ajpcell.00412.2004

(DOI: 10.1152/ajpcell.00412.2004, PubMed: 15601753) Masashi Kuwahata, Yasuko Kuramoto, Yuka Tomoe, Emi Sugata, Hiroko Segawa, Mikiko Ito, Tatsuzo Oka and Ken-ichi Miyamoto :
Posttranscriptional regulation of albumin gene expression by branched-chain amino acids in rats with acute liver injury,
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1739, No.1, 62-69, 2004.

(要約): We previously demonstrated that the integration of albumin mRNA into functional polysomes was regulated by the supply of branched-chain amino acids (BCAA) in the liver of galactosamine-treated rats. To study the mechanism of this regulation, we investigated interaction between rat liver proteins and albumin transcripts. When albumin transcript was incubated with ribosome salt wash (RSW) extracts prepared from liver, a specific RNA-protein complex (p65) formed. Competition experiments showed that a pyrimidine-rich sequence in the coding region of albumin mRNA was required for the formation of p65. The level of p65 was increased in the RSW extracts prepared from liver of galactosamine-treated rats infused with a standard amino acid formula, compared with a BCAA-enriched amino acid formula. The protein in p65 appears to be polypyrimidine tract-binding protein (PTB), because the formation of p65 was reduced in the RSW extracts pre-incubated with anti-PTB antibody. In cell-free translation analysis, immunodepletion of PTB from rabbit reticulocyte lysate caused an increase in albumin translation. These results suggest that binding of PTB to albumin mRNA suppresses its translation. A supply of BCAA may interfere with this binding and improve the translation efficiency of albumin mRNA in injured liver.
(キーワード): Albumin mRNA / Polypyrimidine tract-binding protein / Translation efficiency / Branched-chain amino acid / Acute liver injury
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbadis.2004.08.011
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15607118; ● Search Scopus @ Elsevier (PMID): 15607118; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbadis.2004.08.011

(DOI: 10.1016/j.bbadis.2004.08.011, PubMed: 15607118) Hiroko Segawa, Setsuko Yamanaka, Mikiko Ito, Masashi Kuwahata, Masayuki Shono, Tadashi Yamamoto and Ken-ichi Miyamoto :
Internalization of renal type IIc Na/Pi cotransporter in response to a high phosphate diet,
American Journal of Physiology, Renal Physiology, Vol.288, No.3, 587-596, 2004.

(要約): Dietary phosphate levels regulate the renal brush-border type IIa Na-Pi cotransporter. Another Na-Pi cotransporter, type IIc, colocalizes with type IIa Na-Pi cotransporter in the apical membrane of renal proximal tubular cells. The goal of the present study was to determine whether dietary phosphate levels also rapidly regulate the type IIc Na-Pi cotransporter. Type IIa and type IIc transporter protein levels were increased in rats chronically fed a low-Pi diet compared with those fed a normal-Pi diet. Two hours after beginning a high-Pi diet, type IIa transporter levels were decreased, whereas type IIc protein levels remained unchanged. Western blot analysis of brush-border membrane prepared 4 h after beginning a high-Pi diet showed a significant reduction in type IIc transporter protein levels, and immunohistochemistry showed translocation of the type IIc-immunoreactive signal from the entire brush border to subapical membrane. Membrane fractionation studies revealed a decrease in apical membrane type IIc protein without changes in total cortical type IIc protein, which is compatible with redistribution of type IIc protein from the apical membrane to the dense membrane fraction. The microtubule-disrupting reagent colchicine prevented this reduction in apical type IIc transporter at the apical membrane but had no effect on type IIa transporter levels. These data suggest that the type IIc Na-Pi cotransporter level is rapidly regulated by rapid adaptation to dietary Pi in a microtubule-dependent manner. Furthermore, the mechanisms of the internalization of the type IIc transporter are distinct from those of the type IIa transporter.
(キーワード): Animals / Diet / Down-Regulation / Immunoblotting / Immunohistochemistry / Kidney / Kidney Cortex / Kidney Tubules, Proximal / Male / Membranes / Microscopy, Fluorescence / Microtubules / Microvilli / Peptides / Phosphates / Phosphorus, Dietary / Rats / Rats, Wistar / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Symporters
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00097.2004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15561978; ● Search Scopus @ Elsevier (PMID): 15561978; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00097.2004

(DOI: 10.1152/ajprenal.00097.2004, PubMed: 15561978) Eiji Takeda, Junji Terao, Yutaka Nakaya, Ken-ichi Miyamoto, Yoshinobu Baba, Hiroshi Chuman, Ryuji Kaji, Tetsuro Ohmori and Kazuhito Rokutan :
Stress control and human nutrition,
The Journal of Medical Investigation : JMI, Vol.51, No.3-4, 139-145, 2004.

(要約): Stress is a pervasive factor in everyday life that critically affects development and functioning. Severe and prolonged stress exposure impairs homeostatic mechanisms, particularly associated with the onset of depressive illness. Brain food is aimed at preventing as well as treating a growing number of stress-related mental disorders. Some topics on the association of stress and nutrition is reviewed. (1) An increased activity of serotonergic neurons in the brain is an established consequence of stress. An increase in brain tryptophan levels on the order of that produced by eating a carbohydrate-rich/protein-poor meal causes parallel increases in the amounts of serotonin released into synapses. (2) Eating is thought to be suppressed during stress, due to anorectic effects of corticotrophin releasing hormone, and increased during recovery from stress, due to appetite stimulating effects of residual cortisol. (3) A strong inverse association between coffee intake and risk of suicide. (4) Night eating syndrome has been found to occur during periods of stress and is associated with poor results at attempts to lose weight and disturbances in the hypothalamic-pituitary-adrenal axis. (5) Dietary antioxidants present in fruits and vegetables may improve cognitive function. Therefore, it is concluded that the establishment of functional foods that correctly regulate stress response must be firmly based upon scientific knowledge and legal regulation.
(キーワード): Antioxidants / 脳 (brain) / Coffee / Cognition / Dietary Carbohydrates / Feeding Behavior / Humans / Hydrocortisone / Nutritional Physiological Phenomena / Serotonin / Stress, Physiological / Suicide
(徳島大学機関リポジトリ): ● Metadata: 110734
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.51.139
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15460899; ● Summary page in Scopus @ Elsevier: 2-s2.0-7044220587

(徳島大学機関リポジトリ: 110734, DOI: 10.2152/jmi.51.139, PubMed: 15460899, Elsevier: Scopus) Ken-ichi Miyamoto, Hiroko Segawa, Mikiko Ito and Masashi Kuwahata :
Physiological Regulation of Renal Sodium-Dependent Phosphate Cotransporters,
The Japanese Journal of Physiology, Vol.54, No.2, 93-102, 2004.

(要約): The physiological regulation of renal Pi reabsorption is mediated by renal type II Na/Pi cotransporters (type IIa and type IIc). The type IIa transporter is regulated, among other factors, by dietary Pi intake and parathyroid hormone (PTH). The PTH-induced inhibition of Pi reabsorption is mediated by endocytosis of the type IIa transporter from the brush-border membrane and subsequent lysosomal degradation. Type IIa is part of the heteromeric protein complexes organized by PDZ proteins. Furthermore, during Pi depletion the type IIc Na/Pi cotransporter is induced in the apical membrane of proximal tubular cells. The type IIc transporter is also regulated by PTH via internalization, but by a vesicular transport pathway distinct from that used by the type IIc transporter. Studying the mechanisms of type IIa and type IIc transporters has increased the understanding of the control of proximal tubular Pi handling and thus of overall Pi homeostasis.
(キーワード): kidney / phosphate / transporter / parathyroid hormone
(出版サイトへのリンク): ● Publication site (DOI): 10.2170/jjphysiol.54.93
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15182416; ● CiNii @ 国立情報学研究所 (CRID): 1390001205043873664; ● Search Scopus @ Elsevier (PMID): 15182416; ● Search Scopus @ Elsevier (DOI): 10.2170/jjphysiol.54.93

(DOI: 10.2170/jjphysiol.54.93, PubMed: 15182416, CiNii: 1390001205043873664) Hiroko Segawa, Ichiro Kaneko, Setsuko Yamanaka, Mikiko Ito, Masashi Kuwahata, Yoshio Inoue, Shigeaki Kato and Ken-ichi Miyamoto :
Intestinal Na-Pi cotransporter adaptation to dietary Pi content in vitamin D receptor null mice.,
American Journal of Physiology, Renal Physiology, Vol.287, No.1, F39-F47, 2004.

(要約): Recent studies suggest that vitamin D may play a role in intestinal Na(+)-dependent phosphate transport adaptation to variable levels of dietary P(i). Therefore, the goal of the current study was to assess Na(+)-dependent P(i) cotransport activity in transgenic mice to determine whether vitamin D is an essential mediator of this process. Intestinal brush-border membrane (BBM), Na(+)-dependent P(i) cotransport activity was significantly decreased in vitamin D receptor (VDR) null [VDR (-/-)] mice compared with wild-type (VDR+/+) mice. While intestinal Na-P(i) cotransporter (type IIb) mRNA levels were similar in VDR (-/-) and VDR (+/+) mice, type IIb Na-P(i) cotransporter protein expression was markedly suppressed in VDR (-/-) mice compared with VDR (+/+) mice. Furthermore, Na-P(i) cotransport activity in renal BBM was similar in VDR (-/-) and VDR (+/+) mice, but type IIa Na-P(i) cotransporter protein expression was decreased in VDR (-/-) mice. After administration of a low-P(i) diet, type IIb protein expression was significantly increased in VDR (+/+) and VDR (-/-) mice, and type IIb protein expression was present in the intestinal BBM of VDR (-/-) mice. These data demonstrate that intestinal Na-P(i) cotransport adaptation to a low-P(i) diet occurs independently of vitamin D.
(キーワード): Animals / Diet / Gene Expression Regulation / Genotype / 免疫組織化学 (immunohistochemistry) / Mice / ノックアウトマウス (knockout mice) / Microvilli / Phosphates / Phosphorus, Dietary / Polymerase Chain Reaction / Receptors, Calcitriol / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIb / Symporters / ビタミンD (vitamin D)
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00375.2003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14996670; ● Search Scopus @ Elsevier (PMID): 14996670; ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00375.2003

(DOI: 10.1152/ajprenal.00375.2003, PubMed: 14996670) Mikiko Ito, Sachi Iidawa, Michiyo Izuka, Sakiko Haito, Hiroko Segawa, Masashi Kuwahata, Ichiro Ohkido, Hiroshi Ohno and Ken-ichi Miyamoto :
Interaction of a farnesylated protein with rwnal type a Na/Pi co-transporter in response to parathyroid hormone and dietary phosphate.,
The Biochemical Journal, Vol.377, No.3, 607-616, 2004.

(要約): Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. A dibasic amino acid motif (KR) in the third intracellular loop of the co-transporter is essential for protein's PTH-induced retrieval. To elucidate the mechanism of internalization of Na/P(i) IIa, we identified the interacting protein for the endocytic motif by yeast two-hybrid screening. We found a strong interaction of the Na/P(i) IIa co-transporter with a small protein known as the PEX19 (human peroxisomal farnesylated protein; PxF, Pex19p). PEX19 can bind to the KR motif, but not to a mutant with this motif replaced with NI residues. PEX19 is highly expressed in mouse and rat kidney. Western blot analysis indicates that PEX19 is located in the cytosolic and brush-border membrane fractions (microvilli and the subapical component). Overexpression of PEX19 stimulated the endocytosis of the Na/P(i) IIa co-transporter in opossum kidney cells in the absence of PTH. In conclusion, the present study indicates that PEX19 may be actively involved in controlling the internalization and trafficking of the Na/P(i) IIa co-transporter.
(キーワード): Amino Acid Sequence / Animals / Cell Line / Down-Regulation / Gene Library / Humans / Kidney / Kidney Tubules, Proximal / Male / Membrane Proteins / Mice / Microvilli / Molecular Sequence Data / Opossums / Parathyroid Hormone / Peptides / Phosphates / Rats / Rats, Wistar / シグナル伝達 (signal transduction) / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type IIa / Symporters / Transfection / Two-Hybrid System Techniques
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/BJ20031223
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14558883; ● Search Scopus @ Elsevier (PMID): 14558883; ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20031223

(DOI: 10.1042/BJ20031223, PubMed: 14558883) Mikiko Ito, Iidawa Sachi, Izuka Michiyo, Haito Sakiko, Hiroko Segawa, Masashi Kuwahata, Ohkido Ichiro, Ohno Hiroshi and Ken-ichi Miyamoto :
Cloning and characterization of three PHEX homologues in Drosophila.,
Journal of Bone and Mineral Metabolism, Vol.22, No.1, 3-11, 2004.

(要約): Inactivating mutations and/or deletions of PHEX ( Phosphate-regulating gene with Homologies to Endopeptidase on the X chromosome) are responsible for X-linked hypophosphatemic rickets in humans. In the present study, three Drosophila PHEX homologues (dPHEX-1, -2, -3) were isolated by the screening of a Drosophila cDNA library and expressed sequence tag (EST) database. The structural region involving motif II: (456)WMXXXTKXXAXXK(468) (numbered according to human PHEX), motif VI: (602)WW(603), and motif VIII: (746)CXLW(749) was conserved in the dPHEX family. Zinc-coordinating motifs (HEFTH and GENIADNGG) were also conserved in the dPHEX family. All three dPHEX genes were expressed during all stages of Drosophila development. The expression of dPHEX-1 was suppressed by dietary phosphate deprivation, but the expression of dPHEX-2 and that of dPHEX-3 were not affected. In-situ hybridization showed a ubiquitous distribution of dPHEX-1 and dPHEX-2, while dPHEX-3 was highly expressed in the larval brain. In an analysis of subcellular localization, dPHEX-1 was localized to intracellular organelles and dPHEX-3 was localized predominately in the plasma membrane of Drosophila embryonic S2 cells. Homozygosity of a dPHEX-1 mutation, a transposon insertion in the dPHEX-1 promoter region, was completely lethal at an early stage of embryonic development. The present study indicates that three homologues are likely involved in the phosphate homeostasis of Drosophila.
(キーワード): Alternative Splicing / Amino Acid Sequence / Animals / Base Sequence / Cell Line / Cell Membrane / Cloning, Molecular / Crosses, Genetic / Databases, Nucleic Acid / Drosophila / Drosophila Proteins / Embryo, Nonmammalian / Endoplasmic Reticulum / Exons / Gene Components / Gene Expression / Gene Expression Regulation, Developmental / Genotype / Golgi Apparatus / Homozygote / Humans / Immunohistochemistry / In Situ Hybridization / Microscopy, Fluorescence / Molecular Sequence Data / Mutagenesis, Insertional / PHEX Phosphate Regulating Neutral Endopeptidase / Phosphates / Proteins / Reverse Transcriptase Polymerase Chain Reaction / Sequence Homology, Amino Acid / Transfection
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00774-003-0440-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14691680; ● CiNii @ 国立情報学研究所 (CRID): 1573950399836536704; ● Search Scopus @ Elsevier (PMID): 14691680; ● Search Scopus @ Elsevier (DOI): 10.1007/s00774-003-0440-8

(DOI: 10.1007/s00774-003-0440-8, PubMed: 14691680, CiNii: 1573950399836536704) Naoya Ikeda, Hiroji Uemura, Hitoshi Ishiguro, Mayumi Hori, Masahiko Hosaka, Satoru Kyo, Ken-ichi Miyamoto, Eiji Takeda and Yoshinobu Kubota :
Combination Treatment with 1α,25-Dihydroxyvitamin D₃ and 9-cis-Retinoic Acid Directly Inhibits Human Telomerase Reverse Transcriptase Transcription in Prostate Cancer Cells,
Molecular Cancer Therapeutics, Vol.2, No.8, 739-746, 2003.

(要約): The vitamin D(3) receptor, which is the nuclear receptor for 1alpha,25-dihydroxyvitamin D(3) (VD(3)), forms a heterodimer with the retinoid X receptor (RXR), which is the nuclear receptor for 9-cis-retinoic acid (9-cis-RA). The heterodimer binds to a specific response element consisting of two directly repeated pairs of motifs, AGGTGA, spaced by three nucleotides [direct repeat (DR) 3] and modulates the expression of VD(3)-responsive genes. Telomerase activity, which is seen in most immortal cells and germ cells, is a complex of enzymes that maintain the length of telomeres. One of the major components of human telomerase, human telomerase reverse transcriptase (hTERT), is the catalytic subunit, and the expression of hTERT might correlate most strongly with telomerase activity. We found that the sequence of 5'-AGTTCATGGAGTTCA-3' (DR3') is similar to that of DR3 in the promoter region of hTERT. Our results showed that the combination of VD(3) and 9-cis-RA inhibited telomerase activity through direct interaction of the heterodimer of vitamin D(3) receptor and RXR with the DR3' sequence in the hTERT promoter as well as the combination of VD(3) and selective RXR ligand did. Also, in vivo data showed that the growth of xenografts in nude mice was inhibited by VD(3) and 9-cis-RA. The results of the present study provide evidence on the molecular mechanism of the inhibition of cell growth by these agents, and they could be novel therapeutic agents for prostate cancer.
(キーワード): Animals / Antineoplastic Agents / Calcitriol / DNA-Binding Proteins / Drug Synergism / Humans / Male / Mice / Promoter Regions, Genetic / Prostatic Neoplasms / Reverse Transcriptase Polymerase Chain Reaction / Telomerase / Transcription, Genetic / Tretinoin / Tumor Cells, Cultured
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12939463; ● Search Scopus @ Elsevier (PMID): 12939463

(PubMed: 12939463) Hiroko Segawa, Eri Kawakami, Ichiro Kaneko, Masashi Kuwahata, Mikiko Ito, Kenichiro Kusano, Hitoshi Saito, Naoshi Fukushima and Ken-ichi Miyamoto :
Effect of hydrolysis-resistant FGF23-R179Q on dietary phosphate regulation of the renal type-II Na/Pi transporter.,
Pflügers Archiv : European Journal of Physiology, Vol.446, No.5, 585-592, 2003.

(要約): Fibroblast growth factor 23 (FGF23), a phosphaturic factor, is involved in the regulation of renal inorganic phosphate (Pi) reabsorption. Proteolysis-resistant FGF23 mutants expressed in rodents reduce Pi uptake in both intestine and kidney, independent of parathyroid hormone action. In the present study, we investigated whether FGF23 affects dietary regulation of Na(+)-dependent Pi (Na/Pi) cotransport in the rat kidney using wild-type FGF23 and an R179Q mutant, which disrupts a consensus proteolytic cleavage motif. Rats injected with naked human FGF23 DNA (wild-type or R179Q mutant) expressed the human FGF23 transcript in the liver. In those animals, plasma calcium and parathyroid hormone levels were not affected by FGF23 (either wild-type or R179Q mutant). FGF23-R179Q did, however, significantly decrease plasma Pi and renal Na/Pi cotransport activity and also the level of type-IIc Na/Pi cotransporter protein in brush-border membrane vesicles (BBMVs) from normal rat kidney. Western blot and immunohistochemical analyses in rats fed a low-Pi diet showed the levels of types-IIa and -IIc Na/Pi cotransporters to be markedly increased. After injection of FGF23-R179Q DNA into the rats fed a low-Pi diet, the levels of the types-IIa and -IIc transporter proteins were decreased. The FGF23 mutant thus blunts the signalling of Pi deprivation to the renal type-II Na/Pi cotransporter, suggesting that the FGF23 pathway could be involved in the signalling of dietary Pi.
(キーワード): Animals / カルシウム (calcium) / Fibroblast Growth Factors / 遺伝子発現 (gene expression) / Humans / Hydrolysis / 免疫組織化学 (immunohistochemistry) / Kidney Tubules, Proximal / Male / Mutagenesis, Site-Directed / Parathyroid Hormone / Phosphates / Phosphorus, Dietary / RNA, Messenger / Rats / Rats, Wistar / シグナル伝達 (signal transduction) / Sodium / Sodium-Phosphate Cotransporter Proteins / Sodium-Phosphate Cotransporter Proteins, Type II / Symporters / Vitamin D
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00424-003-1084-1
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12851820; ● Search Scopus @ Elsevier (PMID): 12851820; ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-003-1084-1

(DOI: 10.1007/s00424-003-1084-1, PubMed: 12851820) Yutaka Taketani, Mayumi Nomoto, Hironori Yamamoto, Masashi Isshiki, Kyoko Morita, Hidekazu Arai, Ken-ichi Miyamoto, Shigeaki Kato and Eiji Takeda :
Increase in IP3 and intracellular Ca²⁺ induced by phosphate depletion in LLC-PK₁ cells.,
Biochemical and Biophysical Research Communications, Vol.305, No.2, 287-291, 2003.

(要約): The mechanisms by which Pi depletion rapidly regulates gene expression and cellular function have not been clarified. Here, we found a rapid increase in intracellular ionized calcium [Ca(2+)](i) by phosphate depletion in LLC-PK(1) cells using confocal microscopy with the green-fluorescence protein based calcium indicator "yellow cameleon 2.1." The increase of [Ca(2+)](i) was observed in the presence or absence of extracellular Ca(2+). At the same time, an approximately twofold increase in intracellular inositol 1,4,5-triphosphate (IP(3)) occurred in response to the acute Pi depletion in the medium. Furthermore, 2-aminoethoxydiphenyl borate completely blocked the [Ca(2+)](i) increase induced by Pi depletion. These results suggest that Pi depletion causes IP(3)-mediated release of Ca(2+) from intracellular Ca(2+) pools and rapidly increases [Ca(2+)](i) in LLC-PK(1) cells.
(キーワード): Animals / Boron Compounds / Calcium / Cell Line / Cytoplasm / Inositol 1,4,5-Trisphosphate / Kidney Tubules, Proximal / Kinetics / Microscopy, Confocal / Phosphates / Rats
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/S0006-291X(03)00750-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12745071; ● Search Scopus @ Elsevier (PMID): 12745071; ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-291X(03)00750-2

(DOI: 10.1016/S0006-291X(03)00750-2, PubMed: 12745071) 桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 :
肝障害モデルラットへのBCAA高含有製剤投与による低アルブミン血症改善機構の検討,
日本病態栄養学会誌, Vol.5, No.1, 21-25, 2002年. Hiroko Segawa, Ichiro Kaneko, Akira Takahashi, Masashi Kuwahata, Mikiko Ito, Ohkido Ichiro, Sawako Tatsumi and Ken-ichi Miyamoto :
Growth-related renal Type II Na/Pi cotransporter.,
The Journal of Biological Chemistry, Vol.277, No.22, 19665-19672, 2002.

(キーワード): DEPENDENT PHOSPHATE COTRANSPORTER / BORDER MEMBRANE-VESICLES / AMINO-ACID TRANSPORTER / RAT-KIDNEY / IDENTIFICATION / EXPRESSION / NAPI-2 / REABSORPTION / ONTOGENY / OOCYTES
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M200943200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11880379; ● CiNii @ 国立情報学研究所 (CRID): 1572824501584477568; ● Search Scopus @ Elsevier (PMID): 11880379; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M200943200

(DOI: 10.1074/jbc.M200943200, PubMed: 11880379, CiNii: 1572824501584477568) Eiji Takeda, Kyoko Sakamoto, Kimi Yokota, Maiko Shinohara, Yutaka Taketani, Kyoko Morita, Hironori Yamamoto, Ken-ichi Miyamoto and Mitsuo Shibayama :
Phosphorus supply per capita from food in Japan between 1960 and 1995,
Journal of Nutritional Science and Vitaminology, Vol.48, No.2, 102-108, 2002.

(要約): The awareness of phosphorus intake is important because hyperphosphatemia and hypophosphatemia both impair bone metabolism. Phosphorus consumption from food was obtained from values in the Food Balance Sheet (PBS) of Japan from 1960 to 1995. The amounts of phosphorus calculated from the FBS increased gradually from 1,243 mg/d in 1960 to 1,332 mg/d in 1975 and to 1,421 mg/d in 1995. This is explained by the increased consumption of cow's milk and milk products, meat, and chicken eggs. The main foods supplying phosphorus in 1995 were cereals, milk and milk products, fishes and shellfishes, and vegetables; their contributions were 24.4, 15.8, 14.2, and 10.9%, respectively. The phosphorus-to-calcium ratio calculated from the FBS was 3.51 in 1960, which decreased to 2.89 in 1975 and 2.44 in 1995. Therefore total phosphorus consumption in 1995 was presumably more than 1,500 mg/d when imported food containing phosphorus and the consumption of phosphorus-containing food additives in Japan are also considered. These findings suggest that the phosphorus consumption estimated from the FBS is increasing and that more attention should be paid to the maintenance of healthy bones in Japan, where the average amount of calcium intake is less than 600 mg/d.
(キーワード): Bone and Bones / Calcium, Dietary / Food Analysis / Food Supply / Humans / 日本 (Japan) / Nutritional Requirements / リン (phosphorus) / Phosphorus, Dietary
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12171429; ● Search Scopus @ Elsevier (PMID): 12171429

(PubMed: 12171429) Osamu Yanagida, Yoshikatsu Kanai, Arthit Chairoungdua, Do Kyung Kim, Hiroko Segawa, Tomoko Nii, Seok Ho Cha, Hirotaka Matsuo, Jun-ichi Fukushima, Yoshiki Fukasawa, Yoshiko Tani, Yutaka Taketani, Hiroshi Uchino, Ju Young Kim, Jun Inatomi, Isao Okayasu, Ken-ichi Miyamoto, Eiji Takeda, Tomoyuki Goya and Hitoshi Endou :
Human L-type amino acid transporter 1(LAT1):/characterization of function and expression in tumor cell lines,
Biochimica et Biophysica Acta (BBA) - Biomembranes, Vol.1514, No.2, 291-302, 2001.

(要約): System L is a major nutrient transport system responsible for the transport of large neutral amino acids including several essential amino acids. We previously identified a transporter (L-type amino acid transporter 1: LAT1) subserving system L in C6 rat glioma cells and demonstrated that LAT1 requires 4F2 heavy chain (4F2hc) for its functional expression. Since its oncofetal expression was suggested in the rat liver, it has been proposed that LAT1 plays a critical role in cell growth and proliferation. In the present study, we have examined the function of human LAT1 (hLAT1) and its expression in human tissues and tumor cell lines. When expressed in Xenopus oocytes with human 4F2hc (h4F2hc), hLAT1 transports large neutral amino acids with high affinity (K(m)= approximately 15- approximately 50 microM) and L-glutamine and L-asparagine with low affinity (K(m)= approximately 1.5- approximately 2 mM). hLAT1 also transports D-amino acids such as D-leucine and D-phenylalanine. In addition, we show that hLAT1 accepts an amino acid-related anti-cancer agent melphalan. When loaded intracellularly, L-leucine and L-glutamine but not L-alanine are effluxed by extracellular substrates, confirming that hLAT1 mediates an amino acid exchange. hLAT1 mRNA is highly expressed in the human fetal liver, bone marrow, placenta, testis and brain. We have found that, while all the tumor cell lines examined express hLAT1 messages, the expression of h4F2hc is varied particularly in leukemia cell lines. In Western blot analysis, hLAT1 and h4F2hc have been confirmed to be linked to each other via a disulfide bond in T24 human bladder carcinoma cells. Finally, in in vitro translation, we show that hLAT1 is not a glycosylated protein even though an N-glycosylation site has been predicted in its extracellular loop, consistent with the property of the classical 4F2 light chain. The properties of the hLAT1/h4F2hc complex would support the roles of this transporter in providing cells with essential amino acids for cell growth and cellular responses, and in distributing amino acid-related compounds.
(キーワード): Amino Acid Transport Systems / Amino Acids, Essential / Animals / Antigens, CD / Antigens, CD98 / Carrier Proteins / DNA Probes / DNA, Complementary / Fetus / Humans / Molecular Sequence Data / Oocytes / Protein Biosynthesis / RNA, Complementary / RNA, Messenger / Substrate Specificity / Tumor Cells, Cultured / Xenopus
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/S0005-2736(01)00384-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11557028; ● Search Scopus @ Elsevier (PMID): 11557028; ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2736(01)00384-4

(DOI: 10.1016/S0005-2736(01)00384-4, PubMed: 11557028) Tomoko Nii, Hiroko Segawa, Yutaka Taketani, Yoshiko Tani, Makiko Ohkido, Sachie Kishida, Mikiko Ito, Hitoshi Endou, Yoshikatsu Kanai, Eiji Takeda and Ken-ichi Miyamoto :
) Molecular events involved in up-regulating human Na+-independent neutral amino acid transporter LAT1 during T-cell activation,
The Biochemical Journal, Vol.358, No.3, 693-704, 2001.

(キーワード): elongation / promoter / run-on assay

Takehisa Yamamoto, Ken-ichi Miyamoto, Keiichi Ozono, Yutaka Taketani, Kanako Katai, Akimitsu Miyauchi, Masaaki Shima, Hideki Yoshikawa, Kosei Yoh, Eiji Takeda and Shintaro Okada :
Hypophosphatemic rickets accompanying McCune Albright syndrome: evidence that a humoral factor causes hypophosphatemia,
Journal of Bone and Mineral Metabolism, Vol.19, No.5-6, 287-295, 2001.

(要約): McCune-Albright syndrome (MAS) is sometimes complicated by hypophosphatemia. However, it remains unclear whether a humoral factor is associated with the cause of hypophosphatemia. We isolated cells with mutations of the Gsalpha gene from fibrous bone dysplasia tissues of two MAS patients (MAS cells). Severe combined immunodeficiency (SCID) mice were subjected to experiments using from one of these cells patients. Effects of conditioned media (CM) isolated from MAS cells (MAS-CM) on phosphate transport were investigated by using rat renal slices, the renal cell line OK-B, rat intestinal rings and the human intestinal cell line Caco-2. In addition, the effects of MAS-CM on human sodium-dependent phosphate transporter (NPT2) gene promoter activity expression were investigated in the renal cell line OK-B2400 and were compared with the effects of CM isolated from a patient with oncogenic hypophosphatemic osteomalacia (OHO). MAS cells caused significant hypophosphatemia (P < 0.05) and elevated serum alkaline phosphatase activity (P < 0.05) in SCID mice. The MAS-CM significantly inhibited phosphate uptake in everted intestinal rings (P < 0.01), whereas it had no effect on glucose uptake. The MAS-CM had no effect on either phosphate uptake in the kidney or NPT2 gene promoter activity. In contrast, the CM of the OHO patient significantly inhibited phosphate uptake and NPT2 gene promoter activity. These results indicate that the humoral factor derived from fibrous dysplasia cells of the MAS patient is different to that from OHO patients, because the humoral factor from the MAS patient inhibited phosphate transport not in the kidney but in the intestine.
(キーワード): Adolescent / Adult / Animals / Bacterial Proteins / Cells, Cultured / Culture Media, Conditioned / Female / Fibrous Dysplasia, Polyostotic / GTP-Binding Protein alpha Subunits, Gs / Hot Temperature / Humans / Hypophosphatemia / Hypophosphatemia, Familial / In Vitro Techniques / Jejunum / Kidney / Membrane Transport Proteins / Mice / Mice, SCID / Phosphates / Promoter Regions, Genetic / Rats / Rats, Wistar
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s007740170012
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11498730; ● Search Scopus @ Elsevier (PMID): 11498730; ● Search Scopus @ Elsevier (DOI): 10.1007/s007740170012

(DOI: 10.1007/s007740170012, PubMed: 11498730) Tomoko Nii, Yutaka Taketani, Yoshiko Tani, Ichiro Ohkido, Hiroko Segawa, Hitonori Yamamoto, Kyoko Morita, Kanshi Minamitani, Masanori Minagawa, Toshiyuki Yasuda, Hiroo Niimi, Akimitsu Miyauchi, Ken-ichi Miyamoto and Eiji Takeda :
Direct demonstration of humorally mediated inhibition of the transcription of phosphate transporter in XLH patients,
Clinical and Experimental Nephrology, Vol.5, No.3, 144-152, 2001.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s101570170002
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-17944363928

(DOI: 10.1007/s101570170002, Elsevier: Scopus) Hidekazu Arai, Ken-ichi Miyamoto, Michiko Yoshida, Hironori Yamamoto, Yutaka Taketani, Kyoko Morita, Megumi Kubota, Shigeko Yoshida, Mikiko Ikeda, F Watabe, Y Kanemasa and Eiji Takeda :
The polymorphism in the caudal-related homeodomain protein Cdx-2 binding element in the human vitamin D receptor gene,
Journal of Bone and Mineral Research, Vol.16, No.7, 1256-1264, 2001. Megumi Kubota, Shigeko Yoshida, Mikiko Ikeda, Y Okada, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda :
Association between two types of vitamin d receptor gene polymorphism and bone status in premenopausal Japanese women.,
Calcified Tissue International, Vol.68, No.1, 16-22, 2001.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/BF02684998
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-0347747812

(DOI: 10.1007/BF02684998, Elsevier: Scopus) Kanako Katai, Ken-ichi Miyamoto, Sachie Kishida, Hiroko Segawa, Tomoko Nii, Hiroko Tanaka, Yoshiko Tani, Hidekazu Arai, Sawako Tatsumi, Kyoko Morita, Yutaka Taketani and Eiji Takeda :
Regulation of intestinal Na+-dependent phosphate co-transporters by a low-phosphate diet and 1,25-dihydroxyvitamin D3.,
The Journal of Biochemistry, Vol.343, No.3, 705-712, 1999. Hisami Okumura, Kaori Genjida, Kimi Yokota, Yutaka Taketani, Kyoko Morita, Ken-ichi Miyamoto, Hidenori Miyake, Seiki Tashiro and Eiji Takeda :
Daily pattern of energy metabolism in cirrhosis.,
Nutrition, Vol.15, No.10, 749-754, 1999.

(要約): The daily pattern of energy expenditure and the oxidation rates of carbohydrates, fats, and protein were evaluated by indirect calorimetry in 18 control subjects (Group 1) and 34 cirrhotic patients who were divided into Groups 2a and 2b showing indocyanin green retention rates at 15 min of <30% and 30% or more, respectively. The ratio of resting energy expenditure to basal energy expenditure (%REE) was higher in the cirrhotic patients than in the controls at 8:30 AM and 2:30 PM. The oxidation rates of carbohydrates and fats under fasting conditions in Group 2b patients were respectively lower, and higher than in Group 1 and 2a patients. After the subjects ate, glucose became the substrate preferentially metabolized, and the proportion of fat metabolized was reduced from 82.9+/-5.1% to 43.9+/-21.9% and from 70.7+/-14.1% to 46.8+/-13.9% in the patients with advanced and less advanced cirrhosis, respectively, and from 59.4+/-27.2% to 48.4+/-18.5% in the controls. The fasting concentrations of non-esterified fatty acids in Group 2b were also significantly higher than those in the Group 1 and Group 2a patients. After eating, these concentrations fell and reached similar levels in the patients and controls. These data indicated that the patients with cirrhosis developed the catabolic state of starvation in the morning because of a lack of glycogen stores. Therefore, frequent meal supplementation to prevent early-onset starvation and energy deficiency may be advisable in such patients to maintain a well-nourished condition.
(キーワード): Aged / Basal Metabolism / Calorimetry, Indirect / Dietary Carbohydrates / Dietary Fats / Dietary Proteins / エネルギー代謝 (energy metabolism) / Fasting / Fatty Acids, Nonesterified / Food / Glycogen / Humans / Liver Cirrhosis / Middle Aged / Oxidation-Reduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/S0899-9007(99)00149-5
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10501287; ● Search Scopus @ Elsevier (PMID): 10501287; ● Search Scopus @ Elsevier (DOI): 10.1016/S0899-9007(99)00149-5

(DOI: 10.1016/S0899-9007(99)00149-5, PubMed: 10501287) Hisami Okumura, Eiji Takeda, Kazumi Takata, Emi Shuto, Ken-ichi Miyamoto, Toshiyuki Watanabe, Yoshifumi Kawano, Yoichi Takaue and Yasuhiro Kuroda :
Total parenteral nutrition on energy metabolism in children undergoing autologous peripheral blood stem cell transplantation.,
The Journal of Medical Investigation : JMI, Vol.44, No.3-4, 199-203, 1998.

(要約): The resting energy expenditure (REE) and the respiratory quotient (RQ) were measured longitudinally using indirect calorimetry to examine the effects of total parenteral nutrition (TPN) on energy metabolism in children undergoing autologous peripheral blood stem cell transplantation (PBSCT). There were six children (two males and four females) and the age ranged from five to 13 years (median, eight yrs). The diagnosis included acute lymphocytic leukemia (ALL; 4), neuroblastoma (NBL; 1) and primitive neuroectodermal tumor (PNET; 1). TPN was started after the patients were stabilized following PBSCT (group A; n = 3) or before the initiation of high-dose cytoreductive chemotherapy (HCC) (group B; n = 3). Duration of HCC before PBSCT was identical between the two groups (six to eight days). Average total calorie and protein intake during HCC was significantly higher for group B than for group A. The %REE, the percentage of REE to the predicted basal energy expenditure (BEE), in group A showed 133 +/- 19%, 129 +/- 14% and 146 +/- 11% during three periods of HCC (days -8 to -1 of PBSCT), bone marrow suppression (days 0 to 11 of PBSCT) and bone marrow recovery (days 12 to 22 of PBSCT), respectively. In contrast, those in group B were 10% to 20% lower than those in group A at all periods. Carbohydrate oxidation rates during HCC in group A were significantly lower than those in group B, and those were not different between both groups during post-PBSCT periods. Fat oxidation rates in both groups were similar at all stages of periods. In contrast, protein degradation rates in group A were significantly higher than those in group B at all stages of the period. From these results, we concluded that commencement of TPN administration prior to HCC in the patients undergoing PBSCT provides beneficial effects to maintain better energy metabolic and nutritional status.
(キーワード): Adolescent / Child / Child, Preschool / エネルギー代謝 (energy metabolism) / Female / Hematopoietic Stem Cell Transplantation / Humans / Male / Parenteral Nutrition / Transplantation, Autologous
(徳島大学機関リポジトリ): ● Metadata: 110667
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9597809; ● Summary page in Scopus @ Elsevier: 2-s2.0-0031995075

(徳島大学機関リポジトリ: 110667, PubMed: 9597809, Elsevier: Scopus) Kazumi Takata, Noriko Chiba, Mariko Tawara, Hisami Okumura, Emi Shuto, Ken-ichi Miyamoto, Ichiro Yokota, Junko Matsuda, Yasuhiro Kuroda and Eiji Takeda :
Comparison of energy metabolism in insulin-dependent and non-insulin-dependent diabetes mellitus,
The Journal of Medical Investigation : JMI, Vol.44, No.1-2, 67-71, 1997.

(要約): To compare the metabolic consequences of insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), glycemic control and energy metabolism were evaluated in 18 children displaying IDDM and 19 NIDDM adult patients. With rising concentrations of fasting blood glucose (FBG), hemoglobin A1C and free fatty acid, the percentage of the ratio of resting energy expenditure (REE) to predicted REE expressed as %REE increased and the respiratory quotient (RQ) decreased. The linear regression between RQ and FBG showed the same gradient in IDDM and NIDDM although the RQ in IDDM was always 0.07 lower than that in NIDDM given various FBG concentrations. Those patients whose RQ values were less than 0.7, indicating ketone body production, included 8 (44%) IDDM and 2 (11%) NIDDM patients. These results may explain the relatively greater manifestation of ketoacidosis in IDDM.
(キーワード): Adult / Child / Diabetes Mellitus, Type 1 / Diabetes Mellitus, Type 2 / エネルギー代謝 (energy metabolism) / Humans / Middle Aged
(徳島大学機関リポジトリ): ● Metadata: 111643
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9395720; ● Summary page in Scopus @ Elsevier: 2-s2.0-0031196541

(徳島大学機関リポジトリ: 111643, PubMed: 9395720, Elsevier: Scopus) Hidekazu Arai, Ken-ichi Miyamoto, Yutaka Taketani, Hironori Yamamoto, Yuka Iemori, Kyoko Morita, Takeharu Tonai, Takehiko Nishisho, Shigenobu Mori and Eiji Takeda :
A vitamin D receptor gene polymorphism in the translation initiation codon: effect on protein activity and relation to bone mineral density in Japanese women.,
Journal of Bone and Mineral Research, Vol.12, No.6, 915-921, 1997. Kanako Katai, Hiroko Segawa, Hiromi Sakata-Haga, Kyoko Morita, Hidekazu Arai, Sawako Tatsumi, Yutaka Taketani, Ken-ichi Miyamoto, Setsuji Hisano, Yoshihiro Fukui and Eiji Takeda :
Acute regulation by dietary phosphate of the sodium-dependent phosphate transporter (NaP(i)-2) in rat kidney.,
The Journal of Biochemistry, Vol.121, No.1, 50-55, 1997. Eiji Takeda, K. Takata, H. Yamanaka, Yutaka Taketani, K. Morita, Ken-ichi Miyamoto, Masayuki Shono, S. Teshima and Kazuhito Rokutan :
Vitamin D3 elicits calcium response and activates blood monocyte-derived macrophages from patients with vitamin D dependent rickets type II.,
FEBS Letters, Vol.4, No.364, 157-160, 1996.

(キーワード): Vitamin D3 / monocyte

Eiji Takeda, Kazumi Takata, Hisami Yamanaka, Yutaka Taketani, Kyoko Morita, Ken-ichi Miyamoto, Masayuki Shono, Shigetada Teshima and Kazuhito Rokutan :
Vitamin D3 elicits calcium response and activates blood monocyte-derived macrophages from patients with vitamin D dependent rickets type 2,
FEBS Letters, Vol.396, 157-160, 1996.

(キーワード): vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release

(キーワード): vitamin D dependent rickets type 2 / Vitamin D3 / Non-genomic action / Monocyte-derived macrophage / Calcium response / Superoxide anion release

MISC

金子一郎, 宇賀穂, 塩﨑雄治, 宮本賢一, 瀬川博子 :
生体内リン恒常性を維持するビタミンD作用,
ビタミン, Vol.95, No.56, 280-285, 2021年.

(要約): 無機リン酸(リン)は生体内で多くの生化学反応に必要であるため，血中リン濃度は一定範囲内に維持されている．低リン血症はくる病/骨軟化症の原因となり，高リン血症は慢性腎臓病(CKD)や透析患者において心血管疾患発症のリスクファクターとなる．副甲状腺ホルモン(PTH)や線維芽細胞増殖因子23(FGF23)は，腎臓でのリン再吸収を抑制することでリン利尿ホルモンとして機能している．活性型ビタミンD[1,25(OH) 2D]は小腸でのリン吸収を促進することに加え，PTHやFGF23の産生調節も行い，生体内リン恒常性を保っている． FGF23シグナル活性化は，尿中リン排泄を亢進させ，低リン血症性くる病を引き起こす(FGF23関連低リン血症性くる病)．また，ビタミンD依存性くる病では，小腸でのリン吸収抑制に加えて，成長期における尿中リン排泄の亢進が低リン血症の原因となる．近年，FGF23中和抗体(Burosumab)が開発され，腎臓リン再吸収と1,25(OH) 2D産生を改善することでくる病患者に有益な効果を示し，欧米及び日本でFGF23関連低リン血症性くる病・骨軟化症の治療薬として承認されている．一方，X連鎖性低リン血症性くる病モデル動物を用いた実験では，ビタミンD製剤単独投与でも低リン血症性くる病の症状を改善できることが示された．この作用の特徴は，FGF23が高値を示すにも関わらずリン再吸収の改善がみとめられることである． CKD患者では，しばしば副甲状腺機能亢進や心血管疾患，骨異栄養症など骨ミネラル代謝異常(CKD-MBD: 慢性腎臓病に伴う骨ミネラル代謝異常)が出現する．CKDにおける高リン血症および1,25(OH) 2D低下を予防・治療することで患者のQOLや予後を改善することが報告されている． このように腎臓でのリン再吸収調節は骨ミネラル代謝に極めて重要である．我々は，リンとビタミンD代謝に注目し，疾患の発症および予防を分子レベルで理解することに努めている．
(キーワード): Phosphate / Vitamin D / VDR / Rickets / CKD
(出版サイトへのリンク): ● Publication site (DOI): 10.20632/vso.95.5-6_280
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390574047045835904; ● Search Scopus @ Elsevier (DOI): 10.20632/vso.95.5-6_280

(DOI: 10.20632/vso.95.5-6_280, CiNii: 1390574047045835904) 辰巳佐和子, 藤井理, 宮本賢一 :
高リン食の危険性:インスタント食品，加工食品,
腎と透析, Vol.82, No.6, 809-812, 2017年. 宮本賢一, 竹谷豊 :
食餌性リンによる血管障害,
日本透析医会雑誌, Vol.30, No.1, 128-133, 2015年. 野村憲吾, 塩崎雄治, 宮本賢一 :
リン代謝調節機構の分子メカニズム.,
Anual Review腎臓2013, 2-16, 2013年. Yoshie Yamagata, Ayako Izumi, Fumie Egashira, Ken-ichi Miyamoto and Jun Kayashita :
Determination of a suitable shear rate for thickened liquids easy for elderly to swallow.,
Food Science and Technology Research, Vol.18, No.3, 27-34, 2012.

(出版サイトへのリンク): ● Publication site (DOI): 10.3136/fstr.18.363
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-84866926543

(DOI: 10.3136/fstr.18.363, Elsevier: Scopus) 桑原煩治, 大井彰子, 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 :
リン酸トランスポーターをめぐる最近の話題.,
消化と吸収, Vol.34, No.3, 181-190, 2012年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1572824500599676928

(CiNii: 1572824500599676928) 加藤秀夫, 中坊幸弘, 宮本賢一 :
人体の構造と機能,
栄養生化学(栄養科学シリーズ), 2012年. 瀬川博子, 大井彰子, 宮本賢一 :
リン酸トランスポーターと疾患,
Bio Clinica 腎臓トランスポーター異常による疾患, Vol.Vol26, No.No11, 23-27, 2011年. Akari Ishisaka, Satomi Ichikawa, Hiroyuki Sakakibara, K Mariusz Piskula, Toshiyuki Nakamura, Yoji Kato, Mikiko Ito, Ken-ichi Miyamoto, Akira Tsuji, Yoshichika Kawai and Junji Terao :
Accumulation of orally administered quercetin in brain tissue and its antioxidative effects in rats.,
Free Radical Biology and Medicine, Vol.51, No.7, 1329-1336, 2011.

(要約): Quercetin is widely distributed in vegetables and herbs and has been suggested to act as a neuroprotective agent. Here, we demonstrate that quercetin can accumulate enough to exert biological activity in rat brain tissues. Homogenates of perfused rat brain without detectable hemoglobin contaminants were treated with -glucuronidase/sulfatase and the released quercetin and its methylated form were analyzed using high-performance liquid chromatography (HPLC) with three different detection methods. Both quercetin and the methylated form were detected in the brain of quercetin-administered rats using HPLC-UV and HPLC with electrochemical detection and were further identified using HPLC-tandem mass spectrometry. Oral administration of quercetin (50mg/kg body wt) attenuated the increased oxidative stress in the hippocampus and striatum of rats exposed to chronic forced swimming. The possible transport of quercetin derivatives into the brain tissue was reproduced in vitro by using a rat brain capillary endothelial cell line, a model of the blood-brain barrier. These results show that quercetin could be a potent nutrient that can access the brain and protect it from disorders associated with oxidative stress.
(キーワード): Administration, Oral / Animals / Antioxidants / Blood-Brain Barrier / Brain / Cells, Cultured / Chromatography, High Pressure Liquid / Electrochemical Techniques / Endothelial Cells / Endothelium, Vascular / Glucuronidase / Humans / Male / Methylation / Neurodegenerative Diseases / Oxidative Stress / Quercetin / Rats / Rats, Wistar / Sulfotransferases / Tandem Mass Spectrometry / Tissue Extracts
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.freeradbiomed.2011.06.017
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21741473; ● Search Scopus @ Elsevier (PMID): 21741473; ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2011.06.017

(DOI: 10.1016/j.freeradbiomed.2011.06.017, PubMed: 21741473) 宮本賢一, 古谷順也, 桑原頌冶, 大井彰子, 瀬川博子 :
ペプチドトランスポーターの機能と生理作用,
栄養・食品機能とトランスポーター, 63-80, 2011年. 大井彰子, 野村憲吾, 宮本賢一 :
リン摂取の危険性,
Clinical Calcium, Vol.Vol21, No.o12, 171-174, 2011年. Masashi Kuwahata, Hiroyo Kubota, Saki Amano, Meiko Yokoyama, Yasuhiro Shimamura, Shunsuke Ito, Aki Ogawa, Yukiko Kobayashi, Ken-ichi Miyamoto and Yasuhiro Kido :
Dietary medium-chain triglycerides attenuate hepatic lipid deposition in growing rats with protein malnutrition.,
Journal of Nutritional Science and Vitaminology, Vol.57, No.2, 138-143, 2011.

(要約): The objective of this study was to investigate the effects of dietary medium-chain triglycerides (MCT) on hepatic lipid accumulation in growing rats with protein malnutrition. Weaning rats were fed either a low-protein diet (3%, LP) or control protein diet (20%, CP), in combination with or without MCT. The four groups were as follows: CP-MCT, CP+MCT, LP-MCT, and LP+MCT. Rats in the CP-MCT, CP+MCT and LP+MCT groups were pair-fed their respective diets based on the amount of diet consumed by the LP-MCT group. Rats were fed each experimental diet for 30 d. Four weeks later, the respiratory quotient was higher in the LP-MCT group than those in the other groups during the fasting period. Hepatic triglyceride content increased in the LP groups compared with the CP groups. Hepatic triglyceride content in the LP+MCT group, however, was significantly decreased compared with that in the LP-MCT group. Levels of carnitine palmitoyltransferase (CPT) 1a mRNA and CPT2 mRNA were significantly decreased in the livers of the LP-MCT group, as compared with corresponding mRNA levels of the other groups. These results suggest that ingestion of a low-protein diet caused fatty liver in growing rats. However, when rats were fed the low-protein diet with MCT, hepatic triglyceride deposition was attenuated, and mRNA levels encoding CPT1a and CPT2 were preserved at the levels of rats fed control protein diets.
(キーワード): Animals / Carnitine O-Palmitoyltransferase / Diet, Protein-Restricted / Fasting / Fatty Liver / Gene Expression / Lipid Metabolism / Liver / Male / Oxidation-Reduction / Protein Deficiency / Proteins / RNA, Messenger / Rats / Rats, Wistar / Triglycerides
(出版サイトへのリンク): ● Publication site (DOI): 10.3177/jnsv.57.138
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21697632; ● Search Scopus @ Elsevier (PMID): 21697632; ● Search Scopus @ Elsevier (DOI): 10.3177/jnsv.57.138

(DOI: 10.3177/jnsv.57.138, PubMed: 21697632) 金子一郎, 杉野紗貴子, 瀬川博子, 宮本賢一 :
腎臓と骨代謝関連ホルモン,
THE BONE, Vol.24, No.4, 55-58, 2010年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1010000782037286160

(CiNii: 1010000782037286160) 宮本賢一, 山口誠一, 辰巳佐和子, 木戸慎介, 瀬川博子 :
フォスファトニンとリン,
腎と透析, Vol.69, No.2, 200-202, 2010年. Hiroko Segawa, Setsuko Yamanaka, Yasue Ohno, Akemi Onitsuka, Kazuyo Shiozawa, Fumito Aranami, Junya Furutani, Yuka Tomoe, Mikiko Ito, Masashi Kuwahata, Akihiro Imura, Yoichi Nabeshima and Ken-ichi Miyamoto :
Correlation between hyperphosphatemia and type II Na-Pi cotransporter activity in klotho mice.,
American Journal of Physiology, Renal Physiology, Vol.292, No.2, F769-F779, 2006.

(要約): Recent studies have demonstrated that klotho protein plays a role in calcium/phosphate homeostasis. The goal of the present study was to investigate the regulation of Na-P(i) cotransporters in klotho mutant (kl/kl) mice. The kl/kl mice displayed hyperphosphatemia, high plasma 1,25(OH)(2)D(3) levels, increased activity of the renal and intestinal sodium-dependent P(i) cotransporters, and increased levels of the type IIa, type IIb, and type IIc transporter proteins compared with wild-type mice. Interestingly, transcript levels of the type IIa/type IIc transporter mRNA abundance, but not transcripts levels of type IIb transporter mRNA, were markedly decreased in kl/kl mice compared with wild-type mice. Furthermore, plasma fibroblast growth factor 23 (FGF23) levels were 150-fold higher in kl/kl mice than in wild-type mice. Feeding of a low-P(i) diet induced the expression of klotho protein and decreased plasma FGF23 levels in kl/kl mice, whereas colchicine treatment experiments revealed evidence of abnormal membrane trafficking of the type IIa transporter in kl/kl mice. Finally, feeding of a low-P(i) diet resulted in increased type IIa Na-P(i) cotransporter protein in the apical membrane in the wild-type mice, but not in kl/kl mice. These results indicate that hyperphosphatemia in klotho mice is due to dysregulation of expression and trafficking of the renal type IIa/IIc transporters rather than to intestinal P(i) uptake.
(キーワード): Animals / カルシウム (calcium) / Diet / Endocytosis / Exocytosis / Fibroblast Growth Factors / Glucuronidase / Kidney / Mice / Mice, Mutant Strains / Phosphates / シグナル伝達 (signal transduction) / Sodium-Phosphate Cotransporter Proteins, Type II
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajprenal.00248.2006
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16985213; ● Summary page in Scopus @ Elsevier: 2-s2.0-33846867744

(DOI: 10.1152/ajprenal.00248.2006, PubMed: 16985213, Elsevier: Scopus) 桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 :
肝障害モデルラットのアルブミン遺伝子転写後調節機構と分岐鎖アミノ酸製剤,
必須アミノ酸研究, No.172, 45-50, 2005年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520010380897734784

(CiNii: 1520010380897734784) 庄野正行, 宮本賢一, 多田千代美, 松原智子, 藤井尊 :
Ornithine decarboxylase (ODC)の高感度測定の試み,
臨床検査, Vol.36, No.6, 685-686, 1992年.

(キーワード): Ornithine decarboxylase

総説・解説

宮本賢一 :
巻頭言∼食事に含まれるリンとその代謝∼,
Clinical Calcium, Vol.22, No.10, 11, Megumi Koike, Minori Uga, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa :
Transporters and Novel Regulator of Phosphate Metabolism,
Endocrines, Vol.4, No.3, 607-615, Aug. 2023. 瀬川博子, 小池萌, 塩﨑雄治, 宮本賢一 :
抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性,
実験医学増刊∼栄養・代謝物シグナルと食品機能∼, Vol.40, No.7, 45-50, 2022年3月. 小池萌, 瀬川博子, 宮本賢一 :
リントランスポーターと疾患.,
別冊・医学のあゆみ-トランスポーターのすべて―, Vol.271, No.1, 97-102, 2020年8月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522825129999441536

(CiNii: 1522825129999441536) Sawako Tatsumi, Kanako Katai, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
NAD metabolism and the SLC34 family: evidence for a liver-kidney axis regulating inorganic phosphate.,
Pflügers Archiv : European Journal of Physiology, Vol.471, No.1, 109-122, Sep. 2018.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00424-018-2204-2
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30218374; ● Search Scopus @ Elsevier (PMID): 30218374; ● Search Scopus @ Elsevier (DOI): 10.1007/s00424-018-2204-2

(DOI: 10.1007/s00424-018-2204-2, PubMed: 30218374) 金子一郎, 宮本賢一, 二川健 :
ビタミンDと筋組織,
Clinical Calcium, Vol.27, No.11, 63(1571)-70(1578), 2017年10月. Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto :
Control of phosphate balance by the kidney and intestine.,
Clinical and Experimental Nephrology, Vol.21, No.Suppl 1, 21-26, Nov. 2016.

(要約): The prevention and correction of hyperphosphatemia are major goals of the treatment of chronic kidney disease (CKD)-bone mineral disorders, and thus, Pi balance requires special attention. Pi balance is maintained by intestinal absorption, renal excretion, and bone accretion. The kidney is mainly responsible for the plasma Pi concentration. In CKD, reduced glomerular filtration rate leads to various Pi metabolism abnormalities, and Pi absorption in the small intestine also has an important role in Pi metabolism. Disturbances in Pi metabolism are mediated by a series of complex changes in regulatory hormones originating from the skeleton, intestine, parathyroid gland, and kidney. In this review, we describe the regulation of type II sodium-dependent Pi co-transporters by the kidney and intestine, including the regulation of Pi transport, circadian rhythm, and the vicious circle between salivary Pi secretion and intestinal Pi absorption in animals with and without CKD.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10157-016-1359-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27900568; ● Search Scopus @ Elsevier (PMID): 27900568; ● Search Scopus @ Elsevier (DOI): 10.1007/s10157-016-1359-4

(DOI: 10.1007/s10157-016-1359-4, PubMed: 27900568) Ichiro Kaneko, Hironori Yamamoto, Kayo Ikuta, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto :
Transcriptional regulation of sodium-phosphate cotransporter gene expression.,
Molecular, Genetic, and Nutritional Aspects of Major and Trace Minerals, 437-445, Sep. 2016.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/B978-0-12-802168-2.00036-1
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1016/B978-0-12-802168-2.00036-1

(DOI: 10.1016/B978-0-12-802168-2.00036-1) 濵田康弘, 宮本賢一 :
病態生理と症例から学ぶ輸液ガイド (第4章)症例から学ぶ輸液療法とその管理の実際低リン血症と高リン血症の是正法と輸液管理,
Medical Practice, Vol.32, 204-208, 2015年4月. 宮本賢一, 竹谷豊 :
食餌性リンによる血管障害,
日本透析医学会雑誌, Vol.30, No.1, 128-133, 2015年4月. Hiroko Segawa, Yuji Shiozaki, Ichiro Kaneko and Ken-ichi Miyamoto :
The Role of Sodium-Dependent Phosphate Transporter in Phosphate Homeostasis.,
Journal of Nutritional Science and Vitaminology, Vol.61 Suppl, S119-121, 2015.

(要約): Inorganic phosphate (Pi) is an essential compound for several biologic functions. Pi levels outside the normal range, however, contribute to several pathological processes. Hypophosphatemia leads to bone abnormalities, such as rickets/osteomalacia. Hyperphosphatemia contributes to vascular calcification in patients with chronic kidney disease and hemodialysis patients and is independently associated with cardiac mortality.Pi homeostasis is regulated by the coordinated function of renal and intestinal sodium-dependent phosphate (NaPi) transporters with dietary Pi, parathyroid hormone, 1,25-dihydroxyvitamin D3, and fibroblast growth factor 23. The type II NaPi transporter/SLC34 family, with three members identified to date, is mainly responsible for Pi homeostasis in the body. SLC34A1 and SCL34A3 are predominantly expressed in the kidney, whereas SLC34A2 is expressed in the small intestine. The role of each SLC34 in the body was recently established by studies of gene-targeted mice. Mutation of SLC34A1 causes Fanconi syndrome and mutation of SLC34A3 causes autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. SLC34A2 is thought to be a major intestinal NaPi transporter and mutation of SLC34A2 causes pulmonary alveolar microlithiasis. A detailed understanding of Pi regulation in the body is important toward maintaining health.
(出版サイトへのリンク): ● Publication site (DOI): 10.3177/jnsv.61.S119
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26598821; ● Summary page in Scopus @ Elsevier: 2-s2.0-84950320878

(DOI: 10.3177/jnsv.61.S119, PubMed: 26598821, Elsevier: Scopus) 金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 :
遺伝性リン代謝異常症,
日本腎臓学会誌, Vol.57, No.4, 758-765, 2015年.

(徳島大学機関リポジトリ): ● Metadata: 114834
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1010000781855761042; ● Summary page in Scopus @ Elsevier: 2-s2.0-84938153583

(徳島大学機関リポジトリ: 114834, CiNii: 1010000781855761042, Elsevier: Scopus) Shinsuke Kido, Ichiro Kaneko, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto :
Vitamin D and type II sodium-dependent phosphate cotransporters.,
Contributions to Nephrology, Vol.180, 86-97, May 2013.

(要約): The type II sodium-dependent Pi (NaPi) cotransporters (NaPi-IIa, NaPi-IIb and NaPi-IIc) contribute to renal and intestinal Pi absorption. 1,25-Dihydroxyvitamin D [1,25(OH)2D3] is an important factor for NaPi-II transporters in the small intestine and kidney. In a previous study, low levels of 1,25(OH)2D3 appeared to suppress the expression of renal NaPi cotransporters. We identified a functional vitamin D receptor-responsive element in the human NaPi-IIa and NaPi-IIc genes in renal epithelial cells. In an analysis of vitamin D receptor (VDR)-null mice, we observed early onset of hypophosphatemia. The cause of the hypophosphatemia in VDR-null mice before weaning appeared to be increased plasma parathyroid hormone (PTH) levels during the suckling periods. A rescue diet (high calcium diet) decreased plasma PTH levels in VDR-null mice. The reduced plasma PTH levels normalized the renal Npt2a and Npt2c protein levels in weanling animals. Thus, the dietary intervention completely normalized the expression of the renal Pi transporters (Npt2a/Npt2c) in VDR-null mice, suggesting that the lack of VDR activity was not the cause of the impaired renal Pi reabsorption. In suckling animals, 1,25(OH)2D3 may be essential for the prevention of the phosphaturic action of PTH. In adult animals, 1,25(OH)2D3 is thought to be an important factor for posttranscriptional regulation of the Npt2b gene in the small intestine. Fibroblast growth factor 23 (FGF23) is a novel phosphaturic factor that influences vitamin D metabolism and renal reabsorption of Pi. We characterized the role of the VDR in the action of FGF23 using VDR-null mice. FGF23 reduced renal Pi transport and 25-hydroxyvitamin D 1a-hydroxylase levels by a mechanism that was independent of the VDR. By contrast, the induction of 25-hydroxyvitamin D 24-hydroxylase and the reduction in serum 1,25(OH)2D3 levels induced by FGF23 were dependent on the VDR. Thus, the VDR is not essential for the phosphaturic action of FGF23, but is essential for control of the plasma 1,25(OH)2D3 level. Moreover, FGF23 reduces intestinal NaPi transport activity and Npt2b protein levels by a mechanism that is dependent on the VDR. Klotho functions as a co-receptor for FGF23 and is increased by 1,25(OH)2D3. Klotho induces phosphaturia by inhibiting the renal NaPi-IIa transporter. In this review, we discuss the roles of 1,25(OH)2D3/VDR in the regulation of renal type II NaPi cotransporters in the kidney and small intestine.
(キーワード): Absorption / Animals / Calcitriol / Calcium, Dietary / Familial Hypophosphatemic Rickets / Fibroblast Growth Factors / Gene Expression Regulation / Glucuronidase / Humans / Hypophosphatemia / Intestinal Absorption / Kidney Tubules / Mice / Mice, Knockout / Parathyroid Hormone / Phosphates / Phosphorus, Dietary / Receptors, Calcitriol / Renal Osteodystrophy / Sodium / Sodium-Phosphate Cotransporter Proteins, Type II / Vitamin D
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000346786
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23652552; ● Search Scopus @ Elsevier (PMID): 23652552; ● Search Scopus @ Elsevier (DOI): 10.1159/000346786

(DOI: 10.1159/000346786, PubMed: 23652552) 瀬川博子, 佐々木祥平, 向井朋, 真鍋舞, 木戸慎介, 辰巳佐和子, 宮本賢一 :
リンの体内動態(腸管,腎臓における吸収と排泄機序/リン輸送体の機能作用),
Clinical Calcium, Vol.22, No.10, 13-20, 2012年9月. 桑原頌冶, 野村憲吾, 大井彰子, 宮本賢一 :
FGF23およびKlothoによる尿細管でのリン輸送制御機序,
腎と透析, Vol.72, No.3, 311-315, 2012年3月. Ken-ichi Miyamoto, Sakiko Haito-Sugino, Shoji Kuwahara, Akiko Ohi, Kengo Nomura, Mikiko Ito, Masashi Kuwahata, Shinsuke Kido, Sawako Tatsumi, Ichiro Kaneko and Hiroko Segawa :
Sodium-dependent phosphate cotransporters: lessons from gene knockout and mutation studies.,
Journal of Pharmaceutical Sciences, Vol.100, No.9, 3719-3730, May 2011.

(要約): Inorganic phosphate (Pi) is an essential physiological compound, highlighted by the syndromes caused by hypo or hyperphosphatemic states. Hyperphosphatemia is associated with ectopic calcification, cardiovascular disease, and increased mortality in patients with chronic kidney disease (CKD). As phosphate control is not efficient with diet or dialysis, oral Pi binders are used in over 90% of patients with renal failure. However, achieving tight control of serum Pi is difficult, and lower levels of serum Pi (severe hypophosphatemia) do not lead to better outcomes. The inhibition of sodium-dependent Pi (NaPi) transporter would be a preferable method to control serum Pi levels in patients with CKD or patients undergoing dialysis. Three types of NaPi transporters (types I-III) have been identified: solute carrier series SLC17A1 (NPT1/NaPi-I/OATv1), SLC34 (NaPi-IIa, NaPi-IIb, NaPi-IIc), and SLC20 (PiT1, PiT2), respectively. Knockout mice have been created for types I-III NaPi transporters. In this review, we discuss the roles of the NaPi transporters in Pi homeostasis.
(キーワード): Animals / Gene Knockdown Techniques / ノックアウトマウス (knockout mice) / ノックアウトマウス (knockout mice) / Mutation / Phosphate Transport Proteins / Sodium
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jps.22614
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21567407; ● Search Scopus @ Elsevier (PMID): 21567407; ● Search Scopus @ Elsevier (DOI): 10.1002/jps.22614

(DOI: 10.1002/jps.22614, PubMed: 21567407) 宮本賢一, 中屋豊 :
高リン血症と低リン血症,
循環器医のための知っておくべき電解質異常, 216-220, 2011年5月. 大井彰子, 桑原頌治, 木戸慎介, 宮本賢一 :
リン, 亜鉛, 銅.,
循環器医のための知っておくべき電解質異常, 47-51, 2011年5月. 宮本賢一, 岩本隆宏 :
無機イオン動態とトランスポーター,
トランスポートソームの世界-膜輸送研究の源流から未来へ-, 226-230, 2011年3月. 宮本賢一 :
無機リン酸の生体内代謝, --- 無機リン酸の生体内代謝 ---,
生化学, Vol.78, No.12, 1131-1140, 2006年12月.

(キーワード): Animals / Fibroblast Growth Factors / Glucuronidase / Humans / Hypercalciuria / Hypophosphatemia, Familial / Kidney Tubules, Proximal / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17243634; ● CiNii @ 国立情報学研究所 (CRID): 1520290883151151104; ● Search Scopus @ Elsevier (PMID): 17243634

(PubMed: 17243634, CiNii: 1520290883151151104) 竹谷豊, 山本浩範, 武田英二, 宮本賢一 :
ビタミンDとリン代謝, --- 加齢遺伝子とのかかわり ---,
CLINICAL CALCIUM, Vol.16, No.7, 1137-1142, 2006年7月. 宮本賢一 :
栄養素の構造と機能,
新ガイドライン準拠エキスパート管理栄養士養成シリーズ基礎栄養学[第2版], 96-109, 2006年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1020000781987488259

(CiNii: 1020000781987488259) 宮本賢一, 瀬川博子, 伊藤美紀子 :
リン代謝関連分子の新展開,
判断と治療, Vol.93, No.6, 972-976, 2005年6月.

(キーワード): FGF23 / リン利尿 / PHEX / リントランスポーター

宮本賢一, 伊藤美紀子, 瀬川博子 :
生体のリン調節機構とFGF23,
腎と骨代謝, Vol.18, No.2, 99-104, 2005年. 宮本賢一, 伊藤美紀子, 瀬川博子 :
カルシトニンの腎への作用,
Clinical Calcium, Vol.15, No.3, 478-482, 2005年. 宮本賢一, 伊藤美紀子, 瀬川博子 :
リン酸代謝関連遺伝子群と骨粗鬆症,
CLINICAL CALCIUM, Vol.15, No.5, 783-788, 2005年. 宮本賢一, 瀬川博子, 伊藤美紀子 :
薬理作用と生理作用ー腸管への作用ー,
日本臨牀, Vol.63, No.10, 202-204, 2005年.

(キーワード): 小腸 / カルシウム / マグネシウム / リン / 輸送

宮本賢一, 伊藤美紀子, 瀬川博子, 桑波田雅士 :
副甲状腺ホルモン(PTH)による腎カルシウム，リン，ビタミンD代謝調節について,
THE BONE, Vol.18, No.1, 33-38, 2004年.

(キーワード): 副甲状腺ホルモン / 無機リン酸輸送担体 / 腎近位尿細管 / エンドサイトーシス / ビタミンD / カルシウム
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1010282256868935447

(CiNii: 1010282256868935447) 宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 :
腸管のリントランスポーター,
腎と透析, Vol.55, No.6, 12-16, 2004年.

(キーワード): リン / トランスポーター / 小腸

宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 :
新しいリン調節薬の開発と実用化の可能性,
腎と骨代謝, Vol.17, No.4, 371-377, 2004年.

(キーワード): 高リン血症 / 小腸 / リントランスポーター / 阻害薬

伊藤美紀子, 宮本賢一 :
PHEX遺伝子,
骨粗鬆症治療, Vol.3, No.4, 49-53, 2004年.

(キーワード): PHEX / XLH / フォスファトニン / 石灰化 / リン代謝調節

宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 :
PHEXの真の基質`phosphatonin' とは何か?,
THE BONE, Vol.17, No.5, 77-80, 2003年9月.

(キーワード): フォスファトニン / 低リン血症 / 骨石灰化 / リン再吸収 / 腎臓 / クル病

宮本賢一, 瀬川博子, 伊藤美紀子, 桑波田雅士 :
遺伝性くる病,
臨床雑誌内科, Vol.92, No.1, 89-92, 2003年7月. Ken-ichi Miyamoto, Mikiko Ito, Hiroko Segawa and Masashi Kuwahata :
Molecular targets of hyper-phosphatamia in chronic renal failure,
Nephrology, Dialysis, Transplantation, Vol.18, No.Suppl 3, iii79-iii80, Jun. 2003.

(要約): Dietary phosphate restriction can prevent or retard the progress of chronic renal failure (CRF) and secondary hyperparathyroidism. The klotho gene is involved in the development of a syndrome resembling human ageing, and klotho mutant mice show abnormal calcium/vitamin D metabolism, developing hyperphosphataemia and vascular calcification. Phosphate retention rescues the phenotype of klotho mice. The level of expression of klotho RNA was greatly reduced in the kidneys of all CRF patients. Dietary P(i) restriction induced klotho expression, which enhances the beneficial effect of P(i) restriction in patients with CRF and/or on haemodialysis.
(キーワード): Chronic Renal Failure / Dietary Phosphate / Hyperphosphatacmia / Klotho / Secondary Hyperpara-Thyroidism
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/ndt/gfg1020
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12771308; ● Search Scopus @ Elsevier (PMID): 12771308; ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfg1020

(DOI: 10.1093/ndt/gfg1020, PubMed: 12771308) 宮本賢一, 伊藤美紀子, 桑波田雅士, 瀬川博子 :
リンの消化吸収機構とリン低下薬,
臨床透析, Vol.19, No.1, 29-35, 2003年.

(キーワード): 高リン血症 / とらんすぽーたー / リン吸着薬 / 食事性リン / 小腸

伊藤美紀子, 瀬川博子, 宮本賢一 :
リン輸送とその異常,
医学のあゆみ, 109-111, 2003年. Ken-ichi Miyamoto, Mikiko Ito, Masashi Kuwahata and Hiroko Segawa :
Sensing mechanisms of inorganic phosphate in mammalian cells,
Current Topics in Medical Chemistry, Vol.3, 65-75, 2003. 伊藤美紀子, 瀬川博子, 宮本賢一 :
リン代謝における上皮小体ホルモン(PTH)の役割,
CLINICAL CALCIUM, Vol.12, No.12, 1650-1653, 2002年12月. 宮本賢一, 瀬川博子, 河野智子, 伊藤美紀子, 桑波田雅士, 金井好克 :
アミノ酸トランスポーターの構造機能と栄養学的重要性,
必須アミノ酸研究, Vol.165, 13-19, 2002年11月. 宮本賢一, 桑波田雅士, 瀬川博子, 伊藤美紀子 :
魚油(n-3系脂肪酸)の摂取と疾患予防,
四国医学雑誌, Vol.58, No.4-5, 201-204, 2002年10月.

(キーワード): Fish Oil / Oxidation / Fatty acid / EPA / DHA
(徳島大学機関リポジトリ): ● Metadata: 110552

(徳島大学機関リポジトリ: 110552) Eiji Takeda, Kyoko Morita, Yutaka Taketani, Hironori Yamamoto and Ken-ichi Miyamoto :
Renal handling of phosphate,
Calcium In Internal Medicine, 137-148, 2002. 桑波田雅士, 瀬川博子, 伊藤美紀子, 宮本賢一 :
生体内の無機リン酸感受機構,
腎と骨代謝, Vol.15, No.1, 27-32, 2002年.

(キーワード): リンセンサー / 腎臓 / 脳 / リントランスポーター / 食餌性リン

桑波田雅士, 伊藤美紀子, 瀬川博子, 宮本賢一 :
リン代謝の最近の理解とリン調節薬の将来,
透析療法ネクストII 透析骨症は防げる, 43-48, 2002年.

(キーワード): 高リン血症 / リントランスポーター / リン調節薬 / 腎性骨症 / リンセンサー

桑波田雅士, 宇野和美, 高橋保子, 宮本賢一 :
肝疾患における栄養アセスメント,
日本病態栄養学会誌, Vol.5, No.1, 49-53, 2002年. 伊藤美紀子, 瀬川博子, 桑波田雅士, 宮本賢一 :
リンの代謝調節, --- リントランスポーターの役割 ---,
CLINICAL CALCIUM, Vol.11, No.10, 1297-1301, 2001年10月. Ken-ichi Miyamoto and Mikiko Ito :
Transcriptional regulation of the NPT2 gene by dietary phosphate,
Kidney International, Vol.60, No.2, 412-415, Aug. 2001.

(要約): Dietary phosphate (Pi) is an important regulator for renal Pi reabsorption. The type II sodium-dependent phosphate (Na/Pi) cotransporters (NPT2) are located at the apical membranes of renal proximal tubular cells and major functional transporters associated with renal Pi reabsorption. The yeast one-hybrid system was used to clone a transcription factor that binds to a specific sequence (Pi response element) in the promoter of the NPT2 gene. Two cDNA clones that encoded protein of the mouse transcription factor mu E3 (TFE3) were isolated. TFE3 may participate in the transcriptional regulation of the NPT2 gene by dietary Pi.
(キーワード): Transporter molecules / Yeast one-hybrid system / Transcrip-tion Factor / Proximal Tubules / Pi Response Element / Low Protein Diet / Hyperparathyroidism / TFE3
(出版サイトへのリンク): ● Publication site (DOI): 10.1046/j.1523-1755.2001.060002412.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11473618; ● Summary page in Scopus @ Elsevier: 2-s2.0-0034924184

(DOI: 10.1046/j.1523-1755.2001.060002412.x, PubMed: 11473618, Elsevier: Scopus) 宮本賢一, 伊藤美紀子, 桑波田雅士 :
腎不全骨におけるPTH抵抗性の分子機構,
CLINICAL CALCIUM, Vol.11, No.8, 1014-1018, 2001年8月. 宮本賢一, 伊藤美紀子, 桑波田雅士 :
長期透析患者における栄養管理と食生活の問題点;リンの重要性について,
四国医学雑誌, Vol.57, No.2-3, 35-38, 2001年5月.

(キーワード): Phosphorus / Parathyroid Hormone / Dialysis / ROD
(徳島大学機関リポジトリ): ● Metadata: 110483

(徳島大学機関リポジトリ: 110483) 宮本賢一, 伊藤美紀子 :
二次性副甲状腺機能亢進症とリン代謝,
腎と透析, 11-15, 2001年.

(キーワード): Dietary Phosphate / Secondary Hyperparathyroidism / Hyperphosphatemia

講演・発表

Yuji Shiozaki, Minori Uga, Mizuki Miura, Aoi Komiya, Kazuya Tanifuji, Megumi Koike, Ken-ichi Miyamoto and Hiroko Segawa :
Analysis of regulation of Tmem174 expression by Pi concentration and PTH signaling in opossum kidney cells.,
Physiology, Biology and Pathology of Phosphate Gordon Research Conference, Grand Galvez in Galveston, Texas, United States, Feb. 2023. Yasuhiro Ichida, Daniel Weis, Shuichi Ohtomo, Nadine Kaesler, Christoph Kuppe, Tessai Yamamoto, Naoaki Murao, Hiroko Segawa, Yoshiki Kawabe, Naoshi Horiba, Ken-ichi Miyamoto and Jürgen Floege :
PiT-2 Is the Main Transporter Responsible for Intestinal Phosphate Absorption in Human.,
American Society of Nephrology kidney week2019., Nov. 2019. Hiroko Segawa, Yuki Arima, Ai Hanazaki, Megumi Koike, Kazuya Tanifuji and Ken-ichi Miyamoto :
Intestinal Environmental Control and Renal Protection by Intestinal Alkaline Phosphatase (IAP).,
American Society of Nephrology kidney week2019., Nov. 2019. Tetsuhiko Sato, Megumi Koike, Hiroko Segawa, Ken-ichi Miyamoto and Masafumi Fukagawa :
Possible Clinical Relevance of Growth Hormone-Stimulated α-Klotho Upregulation.,
American Society of Nephrology kidney week2019., Nov. 2019. Sawako Tatsumi, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
Daily oscillation of the plasma inorganic phosphate concentration; Impact of Nampt deficient mice.,
ASN (American Society of Nephrology), Kidney Week 2018, Oct. 2018. T Fujii, Hiroko Segawa, A Hamazaki, K Ikuta, A Kushi, Ichiro Kaneko, Sawako Tatsumi and Ken-ichi Miyamoto :
In Vivo Responses of Phosphorus-Based Food Additives with Different Forms,
American Society of Nephrology Kidney week., Nov. 2017. Sawako Tatsumi, Miyagawa Atsumi, Fujii Osamu, Ogata Mao, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
Hepatectomy-Induced Hypophosphatemia: Mechanisms Underlying Downregulation of Phophate Transport in the Small Intestine.,
American Society of Nephrology. Kidney Week2016., Nov. 2016. Ikuta Kayo, Hiroko Segawa, Yuki Shihoko, Ichiro Kaneko, Hanazaki Ai, Fujii Toru, Kushi Aoi, Sawako Tatsumi and Ken-ichi Miyamoto :
Salivary Pi Handling May Be under the Control of Gastrointestinal Pi Sensing.,
American Society of Nephrology.Kidney Week2016., Nov. 2016. Ken-ichi Miyamoto :
Regulation of Renal Phosphate HandlingInter-organ Communication.,
American Society of Nephrology. Kidney Week2016., Nov. 2016. Ichiro Kaneko, Saini K. Rimpi, Witfield Kerr G., Ito Mikiko, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto, Haussler R. Mark and Jurutka W. Peter :
FGF23: A Nurr1-dependent Phosphaturic Hormone Gene That is Transcriptionally Regulated by 1,25-dihydroxyvitamin D,
XVIII International Congress on Nutrition and Metabolism in Renal Disease 2016, Apr. 2016. Ken-ichi Miyamoto and Yutaka Taketani :
Phosphorus content in daily foods and drinks: Does it matter?,
XVIII International Congress on Nutrition and Metabolism in Renal Desease(ICRNM2016)., Apr. 2016. Ichiro Kaneko, Saini K Rimpi, Whitfield G.Kerr, Mikiko Ito, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto, R.Haussler Mark and W.Jurutka Peter :
A Nurr1-dependent phosphaturic hormonegene that is transcriptionally regulated by 1.25-dihydroxyvitamin D.,
XVIII International Congress on Nutrition and Metabolism in Renal Desease(ICRNM2016), Apr. 2016. Hanazaki Ai, Hiroko Segawa, Ikuta Kayo, Fujii Toru, Ichiro Kaneko, Yuki Shihoko, Nishiguchi Shiori, Notsu Keijiro, Shiozaki Yuji, Sawako Tatsumi and Ken-ichi Miyamoto :
Genetic Deletion of NaPi-2c Rescue Phenotype of klotho Knockout Mice wi thout Improving Severe Hyperphosphat emia.,
American Society of Nephrology Kidney week., Nov. 2015. Yuki Shihoko, Hiroko Segawa, Sasaki Shohei, Ikuta Kayo, Ichiro Kaneko, Fujii Toru, Hanazaki Ai, Nishiguchi Shiori, Keijiro Notsu, Aki Eriko, Shiozaki Yuji, Sawako Tatsumi and Ken-ichi Miyamoto :
Disruption of intestinal alkaline phosphatase (Akp3) affects the phosphate homeostasis.,
ACN2015 Asian Congress of Nutrition., May 2015. Haruna Sakaguchi, Sawako Tatsumi, Ogata Mao, Osamu Fujii, Arakaki Tomohiro, Miyagawa Atsumi, Nagamoto Kenta, Takahama Wako, Hirobata Yukiko, Yasui Akihiro, Ichiro Kaneko, Hiroko Segawa and Ken-ichi Miyamoto :
Bone-kidney axis regulating phosphate homeostasis: Study of osteocyte-ablated mice.,
ACN2015 Asian Congress of Nutrition., May 2015. Ichiro Kaneko, Hsieh Jui-Cheng, Whitfield Kerr G., Hiroko Segawa, Ken-ichi Miyamoto, Haussler R. Mark and Jurutka W. Peter :
1,25-Dihydroxyvitamin D enhances human tryptophan hydroxylase gene expression through vitamin D responsive elements in human brain cells.,
12th Asian Congress of Nutrition 2015, May 2015. Hiroko Segawa, Ichiro Kaneko, Yuji Shiozaki, Sawako Tatsumi and Ken-ichi Miyamoto :
The role of Na+-dependent Phosphate transporters in the body.,
ACN2015 Asian Congress of Nutrition., May 2015. Yutaka Taketani, Masashi Masuda, Hisami Okumura, Sawako Tatsumi, Ken-ichi Miyamoto, Eiji Takeda and Hironori Yamamoto :
Niacin and Chronic Kidney Disease.,
ACN2015 Asian Congress of Nutrition., May 2015. 生田かよ, Hiroko Segawa, 佐々木祥平, Ichiro Kaneko, 塩崎雄治, Sawako Tatsumi and Ken-ichi Miyamoto :
Inorganic Phosphate Handling in Salivary Glands.,
American Society of Nephrology (米国腎臓学会), ペンシルバニアコンベンションセンター(フィラデルフィア), Nov. 2014. Ken-ichi Miyamoto :
Dietary management of phosphate: Gastrointestinal phosphate handling in CKD International Society for Hemodialysis.,
第7回国際血液透析学会議, Apr. 2014. K Nomura, Sawako Tatsumi, A Miyagawa, Y Shiozaki, S Sasaki, Hiroko Segawa and Ken-ichi Miyamoto :
Hepatectomy Hypophosphatemia:A Novel Phosphaturic Factor in the Liver Kidney Axis.,
American Society of Nephrology(46)KIDNEY WEEK2013, Nov. 2013. Shinsuke Kido, Hiroko Segawa, Sawako Tatsumi, Ken-ichi Miyamoto and 他4名 :
Molecular mechanisms of cadmium (Cd) dependent fibroblast growth factor 23 secretion in bone,
Americal Society Nephrology, Kidney Week, Nov. 2012. Sawako Tatsumi, Hiroko Segawa, Shinsuke Kido, Ken-ichi Miyamoto and 他6名 :
Mechanisms of hyperphosphatemia in the osteocyte-abelated mice,
Americal Society Nephrology, Kidney Week, San Diego, Nov. 2012. R Hatano, Hiroko Segawa, A Tamura, Ken-ichi Miyamoto, A Tsukita and S Asano :
The membrane cytoskeletal crosslinker ezrin is essential for the regulation of phosphate homeostasis in the kidney,
Americal Society Nephrology, Kidney Week., Nov. 2012. Ken-ichi Miyamoto, R Ohnishi, S Shiozaki, Hiroko Segawa and Sawako Tatsumi :
Clinical consequences of gene mutations involved in renal phosphate transport,
International Symposium on Epithelial Barrier and Transport 2012, Sep. 2012. Hironori Yamamoto, Otani Ayako, Yokoyama Nozomi, Onishi Rina, Takei Yuichiro, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
Regional Up-regulation of 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1) Gene Is Associated with the Pathogenesis of Ectopic Calcification in the Alpha Klotho Mutant Mice,
2012 Annual Meeting of the American Society for Bone and Mineral Research, Sep. 2012. Nakahashi Otoki, Hironori Yamamoto, Tanaka Sarasa, Kozai Mina, Yutaka Taketani, Ken-ichi Miyamoto, Kato Shigeaki and Eiji Takeda :
Dietary Phosphorus Restriction Up-regulates the Ileal Fibroblast Growth Factor 15 Gene Expression through the Vitamin D Receptor Activation,
2012 Annual Meeting of the American Society for Bone and Mineral Research, Sep. 2012. Hiroko Segawa, J Furutani and Ken-ichi Miyamoto :
Dietary inorganic phosphorus and intestinal peptide absorption,
XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012. T Mukai, Hiroko Segawa, Sawako Tatsumi, Shinsuke Kido, Ken-ichi Miyamoto and 他7名 :
The role of salivary glands in phosphate homeostasis,
XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012. Shinsuke Kido, Y Hashimoto, Hiroko Segawa, Sawako Tatsumi and Ken-ichi Miyamoto :
Muscle atrophy in patients with CKD results from FGF23/Klotho-mediated suppression of Insulin/IGF-I signaling,
XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012. Ken-ichi Miyamoto and Block Geoffrey :
Phosphorus in Food and Preservatives and its Role in Diseases of Kidney and Heart, Bone and Mineral Disorders and Cancer,
International Dietary Phosphorus Consensus Conference, Jun. 2012. Ken-ichi Miyamoto :
Phosphorus Management and Clinical Outcomes,
XVI International Congress on Nutrition and Metabolism in Renal Disease 2012, Jun. 2012. Ken-ichi Miyamoto :
Phosphorus in Food and Preservatives and its Role in Diseases of Kidney and Heart, Bone and Mineral Disorders and Cancer,
International Dietary Phosphorus Consensus Conference, Jun. 2012. Sawako Tatsumi, Y Yamaguchi, T Kamatani, K Nomura, A Yoshimi, Shinsuke Kido, Hiroko Segawa and Ken-ichi Miyamoto :
Inorganic phosphate ion homeostasis;osteocyte-kidney axis,
The1st HDphysiology International SymposiumIntegrative Multi-l Systems Biology for in SilicoCardiology and Pharmacokinetics, Jan. 2012. Hironori Yamamoto, Masashi Masuda, Mina Kozai, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
Regulation of Phosphate Homeostasis by Steroid/thyroid Hormones and Its Receptors,
The International Conference on Food Factors 2011 (ICoFF 2011), Taipei, Taiwan, Nov. 2011. Kengo Nomura, Sawako Tatsumi, Yuji Shiozaki, Seiichi Yamaguchi, Tatsuya Kamatani, Hiroko Segawa, Shinsuke Kido and Ken-ichi Miyamoto :
Post-Hepatectomy Hypophosphatemia in Rats,
Journal of the American Society of Nephrology, Philadelphia, Nov. 2011. Hiroko Segawa, Tomo Mukai, Saori Ohnishi, Shohei Sasaki, Akiko Ohi, Shoji Kuwahara, Shinsuke Kido, Sawako Tatsumi, Yasuko Ishikawa, Otoya Ueda, Naoshi Horiba, Kou-ichi Jishage, Naoshi Fukushima and Ken-ichi Miyamoto :
Role of Sodium-Dependent Phosphate(Pi)Transporter(Npt2b)on Salivary Pi Secretion,
Journal of the American Society of Nephrology, Philadelphia, Nov. 2011. Ryo Hatano, Atsushi Tamura, Hiroko Segawa, Ken-ichi Miyamoto, Sachiko Tsukita and Shinji Asano :
Ezrin Is Essential for the Phosphate Reabeorption in the Renal Proximai Tubule,
Journal of the American Society of Nephrology, Philadelphia, Nov. 2011. Akiko Ohi, Sakiko Haito-Sugino, Mikiko Ito, Yuji Shiozaki, Kengo Nomura, Yuri Kusaka, Shohei Sasaki, Saori Ohnishi, Seiichi Yamaguchi, Shinsuke Kido, Sawako Tatsumi, Hiroko Segawa and Ken-ichi Miyamoto :
Molecular Consequences of the SLC34A3 Mutations of Hereditary Hypophosphatemic Rickets with Hypercalciuria(HHRH),
Journal of the American Society of Nephrology, Philadelphia, Nov. 2011. Jun Guo, Hiroko Segawa, Minlin Liu, Lige Song, F Richard Bringhurst, Ken-ichi Miyamoto, Henry M Kronenberg and Harald Juppner :
Phospholipase C signaling through the PTH/PTHrP receptor is required for serum phosphate homeostasis but not for serum 1,25(OH)2D3,
American Society for Bone and Mineral Reseach, カリフォルニア, Sep. 2011. Tan Vu Van, Yutaka Taketani, Eriko Watari, Tomoyo Kitamura, Ken-ichi Miyamoto, Hironori Yamamoto and Eiji Takeda :
ole of Akt-eNOS Signal Pathway in the Endothelial Dysfunction induced by Chronic Kidney Disease with Hyperphosphatemia.,
American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011. Shoko Ikeda, Hironori Yamamoto, Mina Kozai, Masashi Masuda, Sarasa Tanaka, Otoki Nakahashi, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
Regulation of Renal Sodium-Dependent Phosphate Co-Transporters During Lipopolysaccharide-Induced Acute Inflammation.,
American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011. Hironori Yamamoto, Masashi Masuda, Mina Kozai, Sarasa Tanaka, Otoki Nakahashi, Shoko Ikeda, Hiroko Segawa, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
All-Trans-Retinoic Acid Inhibits Intestinal Phosphate Uptake and Type IIb Sodium-Dependent Phosphate Co-Transporter Gene Expression in Rat.,
American Bone and Mineral Research (ASBMR) annual meeting, San Diego, CA, USA, Sep. 2011. 辰巳佐和子, Seiichi Yamaguchi, Tatsuya Kamatani, Yuji Shiozaki, Kengo Nomura, Yukiko Saito, 木戸慎介, 瀬川博子, 宮本賢一 :
Phosphate Homeostasis in Osteocyte-Ablated Mice.,
ASN, 2010年11月. Masashi Masuda, Hironori Yamamoto, Mina Kozai, Yuichiro Takei, Otoki Nakahashi, Shoko Ikeda, Ayako Otani, Yutaka Taketani, Ken-ichi Miyamoto and Eiji Takeda :
All-Trans Retinoic Acid Maintains the Blood Phosphate Levels through the Positive and Negative Regulation of Type II Sodium-Dependent Phosphate Co-Transporter Family Genes in Kidney and Intestine,
American Society of Nephrology Renal Week 2010, Denver, Colorado, USA, November 16-21, 2010, Nov. 2010. Mina Kozai, Hironori Yamamoto, Masashi Masuda, Yuichiro Takei, Sarasa Tanaka, Yutaka Taketani, Ken-ichi Miyamoto, Shigeaki Kato and Eiji Takeda :
Transrepression of Renal 25-hydroxyvitamin D3 1-hydroxylase (CYP27B1) Gene Expression by Thyroid Hormone Receptor 1,
American Society for Bone and Mineral Research 2010 Annual Meeting, Toronto, Canada, October 15-19, 2010, Oct. 2010. Eiji Takeda, Hidekazu Arai, Hironori Yamamoto, M. Kubota, S. Yoshida, Zhang Honghong, Yutaka Taketani, Kyoko Morita and Ken-ichi Miyamoto :
Human vitamin D receptor gene Expression in intestine and osteoporosis,
The 2nd China-Japan International Conference on Vitamins, Shanghai, Oct. 2001. Hironori Yamamoto, K. Kobayashi, Y. Tani, Yutaka Taketani, Kyoko Morita, Hidekazu Arai, Ken-ichi Miyamoto, S. Kato, J. Pike and Eiji Takeda :
Renal cell-specific regulation of type IIa sodium-dependent phosphate cotranspoter gene expression by 1, 25-dihydroxyvitamin D3,
23rd Annual Meeting of American Society for Bone and Mineral Research, Phoenix,Arizona, Oct. 2001. 木戸慎介, 中川航司, 遠藤逸郎, 坂田雅映, 橋本由衣, 辰巳佐和子, 松本俊夫, 宮本賢一 :
糖尿病症骨症の発症機序の解析:終末糖化産物(AGEs)にんよるCanonical,
第1回骨バイオサイエンス研究会, 宇賀穂, 塩﨑雄治, 小宮蒼, 三浦美月, 原田和, 東彩生, 石川茜, 小池萌, 宮本賢一, 金井好克, 瀬川博子 :
リン代謝調節因子Tmem174によるNaPi2a内在化機序の解明,
第56回日本栄養・食糧学会中国・四国支部大会, 2023年10月. 小宮蒼, 三浦美月, 小池萌, 宇賀穂, 濵口ゆき, 原田和, 東彩生, 石川茜, 塩﨑雄治, 宮本賢一, 瀬川博子 :
リン感受センサーの探索,
第70回日本栄養改善学会学術総会, 2023年9月. 宇賀穂, 佐々木すみれ, 三浦美月, 原田和, 小宮蒼, 東彩生, 石川茜, 小池萌, 塩﨑雄治, 金井好克, 宮本賢一, 瀬川博子 :
高リン血症を予防する新規リン代謝調節因子の同定,
第267回徳島医学会学術集会, 2023年8月. 三浦美月, 佐々木すみれ, 塩﨑雄治, 小池萌, 宇賀穂, 東彩生, 長谷川智香, 網塚憲生, 宮本賢一, 瀬川博子 :
Tmem174はリン酸トランスポーターを調節し高リン血症を予防する新規リン代謝調節分子である,
第41回日本骨代謝学会学術集会, 2023年7月. 三浦美月, 小池萌, 宇賀穂, 小宮蒼, 原田和, 東彩生, 小池萌, 宮本賢一, 瀬川博子 :
Tmem174はリン酸トランスポーターを調節し高リン血症を予防する新規リン代謝調節分子である,
第8回日本栄養改善学会四国支部学術総会, 2023年5月. 宇賀穂, 塩﨑雄治, 三浦美月, 小宮蒼, 原田和, 小池萌, 宮本賢一, 瀬川博子 :
新規高リン血症抑制因子Tmem174 の発現調節機構の解明,
第77回日本栄養・食糧学会大会, 2023年5月. 塩﨑雄治, 濱口ゆき, 村本愛奈, 谷藤和也, 宇賀穂, 三浦美月, 小宮蒼, 小池萌, 宮本賢一, 瀬川博子 :
高リン負荷誘導性老化に対抗するXPR1 依存的細胞内リン酸排出機構の解明,
第77回日本栄養・食糧学会大会, 2023年5月. 三浦美月, 佐々木すみれ, 塩﨑雄治, 谷藤和也, 小池萌, 宇賀穂, 宮本賢一, 瀬川博子 :
Tmem174 はリン酸トランスポーターを調節し高リン血症を予防する.,
第7回日本CKD-MBD学会学術集会・総会, 2023年3月. 佐々木すみれ, 塩﨑雄治, 小池萌, 谷藤和也, 宇賀穂, 宮本賢一, 瀬川博子 :
Tmem174はリン酸トランスポーターを調節し高リン血症を予防する,
第95回日本生化学会大会, 2022年11月. 三浦美月, 佐々木すみれ, 小池萌, 谷藤和也, 宇賀穂, 小宮蒼, 濱口ゆき, 原田和, 塩﨑雄治, 宮本賢一, 瀬川博子 :
ポリリン酸は，モノリン酸よりも腎障害およびFGF23分泌に大きな影響を与える,
第69回日本栄養改善学会学術総会, 2022年9月. 瀬川博子, 塩﨑雄治, 金子一郎, 宮本賢一 :
リンが関する生体機能ー成長，疾患，寿命ー,
第76回日本栄養・食糧学会大会シンポジウム 4 ミネラルの新機能, 2022年6月. 有馬佑貴, 瀬川博子, 花崎愛, 佐々木すみれ, 小池萌, 谷藤和也, 野沢愛, 金子一郎, 宮本賢一 :
Intestinal Alkaline Phosphatase(IAP)による腸管リン代謝制御と腎保護作用.,
第52回日本栄養・食糧学会中国・四国支部大会., 2019年10月. 瀬川博子, 有馬佑貴, 小池萌, 谷藤和也, 佐々木すみれ, 花崎愛, 金子一郎, 宮本賢一 :
Intestinal Alkaline Phosphatase(IAP)による腸内環境制御と腎保護作用.,
第66回日本栄養改善学会学術総会., 2019年9月. 金子一郎, 瀬川博子, 加藤茂明, 宮本賢一 :
ビタミンDによる小腸リン輸送調節機序の解明.,
第66回日本栄養改善学会学術総会., 2019年9月. 辰巳佐和子, 中辻翔也, 河田美紀, 桑原煩治, 金子一郎, 瀬川博子, 宮本賢一 :
腸管ニコチンアミドホスホリボシルトランスフェラーゼのリン吸収抑制効果の検討.,
第66回日本栄養改善学会学術総会., 2019年9月. 中辻翔也, 桑原煩治, 室岡響, 田口裕子, 古川菜摘, 森由貴, 古澤みなみ, 瀬川博子, 宮本賢一, 辰巳佐和子 :
高リン血症におけるリン管理:Nampt/NAD代謝の検討.,
第7回日本腎栄養代謝研究回学術集会・総会., 2019年7月. 金子一郎, Haussler R. Mark, Jurutka W. Peter, 瀬川博子, 宮本賢一 :
ビタミンDとうつ病の関係:セロトニン代謝の関係,
第7回日本腎栄養代謝研究会学術集会・総会, 2019年7月. 桐野留里, 瀬川博子, 花崎愛, 佐々木すみれ, 小池萌, 谷藤和也, 金子一郎, 宮本賢一 :
Intestinal Alkaline Phosphatase(IAP)による内環境制御と腎保護作用.,
第3回日本Uremic Toxin研究会学術集会., 2019年4月. 金子一郎, 瀬川博子, 張哲然, 加藤茂明, 宮本賢一 :
ビタミンDが制御する小腸リン吸収機序の解明,
第3回CKD-MBD研究会学術集会・総会, 2019年3月. 篠原理沙, 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 :
骨細胞除去による無機リン代謝における影響:骨-腎臓-腸管連関の解析,
第57回日本栄養・食糧学会近畿支部会, 2018年12月. 宮本賢一 :
透析患者におけるリンの栄養管理,
第49回徳島透析療法研究会, 2018年11月. 宮本賢一 :
CKDにおけるミネラル管理:りん毒性の話題,
第34回京都透析症例検討会, 2018年11月. 谷藤和也, 瀬川博子, 生田かよ, 花崎愛, 佐々木すみれ, 小池萌, 金子一郎, 石川康子, 宮本賢一 :
食物無機リン酸適応唾液-腸管-腎臓ネットワーク,
第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月. 宮本賢一 :
慢性腎臓病におけるミネラル管理,
第5回CKD-MBDエキスパートと語る会, 2018年11月. 宮本賢一 :
リン管理と栄養:消化吸収からの考察,
第9回南空地・江別透析懇談会, 2018年10月. 辰巳佐和子, 齋満帆, 中辻翔也, 河田美紀, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 :
血中リン濃度を上げない食事時間とは?:動物モデルでの検討,
第6回日本腎栄養代謝研究会学術集会・総会, 2018年7月. 宮本賢一, 木戸慎介, 辰巳佐和子, 金子一郎, 瀬川博子 :
カドミウム暴露と骨軟化症:バイオマーカーの探索,
第5回日本栄養改善学会四国支部学術総会, 2018年6月. 張哲然, 金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 加藤茂明, 宮本賢一 :
ビタミンDによる小腸リン吸収促進機構の解明,
第5回日本栄養改善学会四国支部学術総会, 2018年6月. 金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 張哲然, 加藤茂明, 宮本賢一 :
ビタミンDが制御する腸管リン吸収機序の解明,
日本ビタミン学会第70回大会, 2018年6月. 宮本賢一 :
わかりやすいミネラルの代謝と重要性,
2018年度日本栄養改善学会第14回中国支部学術総会, 2018年6月. 金子一郎, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 張哲然, 加藤茂明, 宮本賢一 :
ビタミンDが制御する腸管リン吸収機序の解明,
第72回日本栄養・食糧学会大会, 2018年5月. 瀬川博子, 古谷順也, 金子一郎, 宮本賢一 :
FGF23-リンによる腸管窒素吸収調節,
第2回日本UremicToxin 研究学術集会, 2018年4月. 瀬川博子, 金子一郎, 宮本賢一 :
腎臓と他の臓器相関による生体内リン代謝調節機構,
第95回日本生理学会大会, 2018年3月. 宮本賢一 :
低リン血症と代謝障害:最近の知見,
第37回ROD-21研究会, 2018年1月. 辰巳佐和子, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 :
ミネラル代謝における骨細胞減少の効果:骨細胞-腎臓-腸管連関制御,
第72回日本栄養・食糧学会大会, 2017年11月. 金子一郎, G K.Saini Rimpi, Whitfield Kerr, 伊藤美紀子, 瀬川博子, 辰巳佐和子, 宮本賢一, R.Haussler Mark, W.Jurutka Peter :
リン利尿因子FGF23の転写調節機序の解明,
第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月. 木下瑛美, 辰巳佐和子, 藤井理, 張哲然, 金子一郎, 瀬川博子, 宮本賢一 :
腸管NAD+合成律速酵素(Nampt)と全身性NAD+代謝,
第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月. 宮本賢一 :
リン代謝における多臓器連関:最近の知見,
第9回二次性副甲状腺機能亢進症に伴うPTx研究会学術集会, 2017年10月. 佐々木すみれ, 瀬川博子, 桐野留里, 金子一郎, 辰巳佐和子, 宮本賢一 :
形態の異なるリン化合物接種に対する生体への影響,
第64回日本栄養改善学会学術総会, 2017年9月. 桐野留里, 瀬川博子, 佐々木すみれ, 金子一郎, 辰巳佐和子, 宮本賢一 :
生体内リン恒常性における腸管アルカリフォスファターゼの役割,
第64回日本栄養改善学会学術総会, 2017年9月. 金子一郎, 瀬川博子, 辰巳佐和子, 宮本賢一 :
脳機能における活性型ビタミンDの役割,
第64回日本栄養改善学会学術総会, 2017年9月. 藤井理, 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 :
水溶性ビタミンB3と腸管上皮機能,
第64回日本栄養改善学会学術総会, 2017年9月. 桐野留里, 瀬川博子, 金子一郎, 辰巳佐和子, 宮本賢一 :
生体内リン恒常性におけるアルカフォスファターゼの役割,
第4回日本栄養改善学会四国支部学術総会, 2017年6月. 宮本賢一 :
血中リン濃度維持機構とその破綻:多臓器連関について,
Triology Conference2, 2017年6月. 瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 :
生体内リン恒常性における Intestinal Alkaline Phosphatase (IAP) の役割.,
第71回日本栄養·食糧学会大会, 2017年5月. 辰巳佐和子, 緒方雅央, 新垣友啓, 藤井理, 金子一郎, 瀬川博子, 宮本賢一 :
骨ー腎臓連関を介した食餌性リン感受機Sensing of dietary phosphate loading in the bone-kidney axis.,
第71回日本栄養·食糧学会大会, 2017年5月. 瀬川博子, 金子一郎, 辰巳佐和子, 宮本賢一 :
栄養素輸送担体と健康・疾患「腸管リン吸収と慢性腎臓病」,
第71回日本栄養·食糧学会大会, 2017年5月. 瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 :
生体内リン恒常性におけるIntestinal Alkaline Phosphatase(IAP)の役割,
第1回CKD‐MBD研究会学術集会・総会, 2017年3月. 高濱和子, 辰巳佐和子, 宮川淳美, 藤井理, 新垣友啓, 緒方雅央, 木下瑛美, 金子一郎, 瀬川博子, 宮本賢一 :
リン代謝動態の概日リズム形成機序解明,
第49回日本栄養・食糧学会中国・四国支部大会, 2016年11月. 金子一郎, Hsieh Jui-Cheng, Whitfield Kerr G., 辰巳佐和子, 瀬川博子, 宮本賢一 :
脳機能におけるビタミンDの役割,
第68回日本ビタミン学会, 2016年6月. 川端優佳, 瀬川博子, 結城志帆子, 中山彰吾, 藤井公, 生田かよ, 花崎愛, 野津圭二郎, 西口詩織, 金子一郎, 辰巳佐和子, 宮本賢一 :
形態の異なるリン化合物接種に対する生体への影響,
第70回日本栄養・食糧学会大会, 2016年5月. 瀬川博子, 佐々木祥平, 結城志帆子, 金子一郎, 辰巳佐和子, 宮本賢一 :
生体内リン恒常性におけるIntestinal Alkaline Phosphatase(IAP)の役割,
第1回CKD‐MBD研究会学術集会・総会, 2016年3月. 金子一郎, Jui-Cheng Hsieh, G.Kerr Whitfield, 辰巳佐和子, 瀬川博子, 宮本賢一, R Mark Haussler, W Peter Jurutka :
脳機能におけるビタミンDの役割について,
第19会日本病態栄養学会年次学術集会, 2016年1月. 西口詩織, 瀬川博子, 蓑島さくら, 桑原煩治, 金子一郎, 前田彰, 辰巳佐和子, 宮本賢一 :
リン血症是正に対するFGF23/Klothoシグナルの解明,
第19会日本病態栄養学会年次学術集会, 2016年1月. 新垣友啓, 辰巳佐和子, 緒方雅央, 阪口晴菜, 安井朗洋, 藤井理, 永元健太, 金子一郎, 瀬川博子, 宮本賢一 :
骨細胞の減少による胆汁酸代謝異常についての解析.,
第19会日本病態栄養学会年次学術集会., 2016年1月. 安井朗洋, 辰巳佐和子, 宮本賢一 :
骨細胞欠損マウスにおけるFGF19ファミリーシグナル経路の破綻.,
第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, 2015年12月. 生田かよ, 瀬川博子, 結城志帆子, 金子一郎, 西口詩織, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 :
生体内リン代謝調節機構における唾液腺の関与.,
第38回日本分子生物学会年会・第88回日本生化学会大会合同大会, 2015年12月. 花崎愛, 瀬川博子, 福尾真理, 金子一郎, 辰巳佐和子, 宮本賢一 :
Klotho and NaPi-2c,double deletionから導くNaPi-2cの重要性.,
第48回日本栄養・食糧学会中国・四国支部大会, 2015年10月. 瀬川博子, 森絢加, 宮本賢一, 伊藤美紀子 :
リン排泄分子としてのXenotropic and polytropic retrovirus receptor(XPR)1,
第34回腎と骨代謝研究会学術集会, 2015年10月. 宮川敦美, 辰巳佐和子, 永元健太, 宮本賢一 :
慢性腎臓病による高リン血症改善におけるナイアシンの効果,
第62回日本栄養改善学会学術総会, 2015年9月. 松尾明, 飯田聡夫, 谷本美奈子, 剣持佑介, 柿本恒知, 松下睦佳, 宮本賢一 :
新規リン吸着薬リオナ錠(クエン酸第二鉄水和物製剤)の有効性に関わる有用性検討―非臨床評価―,
第3回日本腎不全栄養研究会学術集会・総会, 2015年7月. 桑原三恵子, 坂内堅二, 瀬川博子, 宮本賢一 :
ラット腎不全初期の心臓リモデリングにおける尿毒素物質の影響.,
第3回日本腎不全栄養研究会学術集会・総会., 2015年7月. 瀬川博子, 金子一郎, 宮本賢一 :
慢性腎臓病におけるリンコントロール.,
第31回日本DDS学会学術集会., 2015年7月. 宮本賢一, 辰巳佐和子 :
肝臓切除因子による高リン血症抑制機序の解明,
第60回日本透析医学会学術集会・総会., 2015年6月. 宮本賢一, 辰巳佐和子, 濵田康弘 :
Clinical Nutrition education in Japanese dietitians.,
第60回日本透析医学会学術集会・総会., 2015年6月. 桑原三恵子, 坂内堅二, 瀬川博子, 宮本賢一, 大和英之 :
ラット腎不全初期における心臓モデリングには尿素毒素物質が影響している,
第5回腎不全研究会, 2014年12月. 瀬川博子, 生田かよ, 塩崎雄治, 金子一郎, 宮本賢一 :
Gastrointestinal phosphate handling.,
上皮バリア・輸送に関するシンポジウム, 2014年11月. 緒方雅央, 辰巳佐和子, 藤井理, 阪口晴菜, 新垣友啓, 宮川淳美, 永元健太, 高濱和子, 廣畠佑希子, 金子一郎, 瀬川博子, 宮本賢一 :
骨細胞除去マウスのカルシウム/リン代謝異常解析について,
第47回日本栄養・食糧学会中国・四国支部大会, 2014年10月. 小林謙一, 志賀孝宏, 滝拓也, 石井京子, 石田香織, 河田哲典, 瀬川博子, 宮本賢一, 竹谷豊, 田所忠弘, 松井芳光, 山本祐司 :
ビタミンB12欠乏が腎臓におけるビタミンDや無機リンの再吸収に及ぼす影響,
第87回日本生化学会大会，平成26年10月15日—10月18日，国立京都国際会館, 2014年10月. 辰巳佐和子, 野村憲吾, 宮川淳美, 永元健太, 藤井理, 瀬川博子, 宮本賢一 :
肝臓切除に伴う低リン血症発症機構の解明:ニコチンアミドホスホリボシルトランスフェラーゼ(Nampt)を介した全身性リン代謝制御機構についての検討.,
第32回日本骨代謝学会学術集会, 2014年7月. 辰巳佐和子, 野村憲吾, 宮川淳美, 永元健太, 藤井理, 瀬川博子, 宮本賢一 :
ニコチンアミドホスホリボシルトランスフェラーゼ(Nampt)を介した全身性リン代謝制御機構についての検討.,
第57回日本腎臓学会学術総会, 2014年7月. 齋藤直朗, 李敏啓, 辰巳佐和子, 池田恭治, 網塚憲生, 小林正治, 宮本賢一 :
骨細胞特異的死滅マウスの骨小腔基質溶解における微細構造学的検索.,
第34回日本骨形態計測学会., 2014年6月. 宮本賢一, 濵田康弘 :
腎臓病専門栄養師の設立に向けて,
第59回日本透析医学会学術集会・総会., 2014年6月. 宮本賢一, 濵田康弘 :
【ワークショップ】腎臓病専門栄養士設立にむけて,
第59回日本透析医学会, 2014年6月. 宮川淳美, 辰巳佐和子, 野村憲吾, 永元健太, 瀬川博子, 宮本賢一 :
NAD合成律速酵素Namptを介したリン代謝制御機構.,
第68回日本栄養・食糧学会大会., 2014年6月. 生田かよ, 瀬川博子, 向井朋, 佐々木祥平, 森絢香, 花崎愛, 森藤久美子, 安井可奈子, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 :
生体内リン代謝調節機構における唾液腺の関与,
第68回日本栄養・食糧学会大会., 2014年6月. 瀬川博子, 宮本賢一 :
リン代謝調節機序におけるNaPiトランスポーターの役割.,
日本農芸化学会2014年度(平成26年度)大会, 2014年3月. 宮本賢一 :
リン過剰摂取が招く危険性と最新の代謝機構,
第22回北摂四医師会骨・内分泌・代謝研究会, 2014年3月. 宮本賢一 :
リン管理と栄養:最新の知見,
CKD患者のリン管理を考える会 in 倉敷, 2014年3月. 宮本賢一 :
栄養の吸収と代謝,
第34回メディコピア教育講演シンポジウム栄養と食欲∼病態と治療の進歩∼, 2014年1月. 辰巳佐和子, 藤田みゆき, 藤井理, 野村憲吾, 瀬川博子, 宮本賢一, 木戸慎介 :
骨細胞死滅マウスにおけるカルシウム/リン代謝異常機構について.,
第17回日本病態栄養学会年次学術集会, 2014年1月. 宮本賢一 :
生体内リン恒常性維持機構の破綻と疾患,
平成25年度戦略的研究推進プログラム次世代重点研究プログラム:Transcriptotherapeuticsの創出と医療への展開., 2013年12月. 野村憲吾, 辰巳佐和子, 宮川淳美, 塩崎雄治, 瀬川博子, 宮本賢一 :
肝臓切除による無機リン酸恒常性破綻機構について,
第36回日本分子生物学会年会, 2013年12月. 宮本賢一 :
リン管理と栄養:最近の知見,
高リン血症治療セミナー., 2013年10月. 宮本賢一 :
保存期におけるリン管理:最近の知見,
旭川高リン血症治療学術講演会, 2013年10月. 宮本賢一 :
透析患者におけるリン管理と栄養摂取.,
第45回西播透析医会, 2013年9月. 辰巳佐和子, 野村憲吾, 大西律子, 宮本賢一 :
肝臓切除患者における低リン血症発症機序の解明,
第60回日本栄養改善学会学術総会, 2013年9月. 大西律子, 谷佳子, 山田静恵, 松村晃子, 宮本賢一 :
食道癌術後乳糜胸をオクトレオチドと低脂肪食の栄養治療で回復した一例.,
第60回日本栄養改善学会学術総会, 2013年9月. 生田かよ, 瀬川博子, 向井朋, 佐々木祥平, 森絢加, 石川康子, 上田乙也, 堀場直, 寺社下浩一, 福島直, 宮本賢一 :
生体内リン代謝調節機構における唾液腺の関与.,
第86回日本生化学会大会, 2013年9月. 塩崎雄治, 瀬川博子, 大西沙織, 大井彰子, 杉野紗貴子, 簑島さくら, 伊藤美紀子, 木戸慎介, 辰巳佐和子, 宮本賢一 :
近位尿細管上皮細胞におけるNa+依存性無機リン酸輸送担体Npt2cの発現調節とVacuole形成,
第86回日本生化学会大会, 2013年9月. 宮本賢一 :
食品添加物としてのリン:最近の話題,
第13回東京腎不全骨代謝研究会∼透析患者さんのリンの管理∼, 2013年7月. 宮本賢一 :
リンの話題:栄養とリン調節薬.,
第12回徳島腎と薬剤研究会, 2013年7月. 宮本賢一 :
慢性腎臓病におけるリン代謝異常:炭酸ランタンの有効性について,
第24回日本微量元素学会学術集会, 2013年6月. 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 :
骨とリン利尿因子,
第58回日本透析医学会学術集会・総会, 2013年6月. 木戸慎介, 越智美佐子, 藤原真理奈, 向井朋, 塩崎雄治, 瀬川博子, 辰巳佐和子, 宮本賢一 :
慢性腎臓病に併存する骨ミネラル代謝障害(CKD-MBD)の発症並びに進展におけるFGF23の関与.,
第67回日本栄養・食糧学会大会, 2013年5月. 宮川淳美, 辰巳佐和子, 野村憲吾, 木戸慎介, 瀬川博子, 宮本賢一 :
Nampt+/-のリン代謝の解析,
第67回日本栄養・食糧学会大会, 2013年5月. 野村憲吾, 辰巳佐和子, 宮川淳美, 岡奈都紀, 塩崎雄治, 木戸慎介, 瀬川博子, 佐野光枝, 福渡努, 柴田克己, 宮本賢一 :
肝臓切除患者における低リン血症発症機構の解明.,
第67回日本栄養・食糧学会大会, 2013年5月. 佐々木祥平, 瀬川博子, 大西沙織, 森絢加, 向井朋, 真鍋舞, 日下祐里, 木戸慎介, 辰巳佐和子, 宮本賢一 :
リン利尿におけるKlothoの役割,
第56回日本腎臓学会学術総会, 2013年5月. 桑原三恵子, 坂内堅二, 菊池香織, 大和英之, 瀬川博子, 宮本賢一 :
腎機能低下に伴う心肥大には血圧以外に尿毒素物質が関与している.,
第56回日本腎臓学会学術総会, 2013年5月. 辰巳佐和子, 釜谷達哉, 宮本賢一 :
骨細胞死滅マウスにおけるリン利尿促進機序について.,
第56回日本腎臓学会学術総会, 2013年5月. 佐々木祥平, 瀬川博子, 大西沙織, 森絢加, 向井朋, 真鍋舞, 日下祐里, 木戸慎介, 辰巳佐和子, 宮本賢一 :
リン利尿におけるKlothoの役割.,
第56回日本腎臓学会学術総会, 2013年5月. 宮本賢一 :
リン管理と栄養:最新の知見,
CKD患者のリン管理を考える会, 2013年3月. 日下祐里, 瀬川博子, 木戸慎介, 辰巳佐和子, 宮本賢一, 他5名 :
腸管リン吸収における腸アルカリフォスファターゼの役割,
第16回日本病態栄養学会年次学術集会, 2013年1月. 大西律子, 宮本賢一, 他12名 :
食道癌術後乳糜胸をオクトレオチドと低脂肪の栄養治療で回復した一例,
第16回日本病態栄養学会年次学術集会, 2013年1月. 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一, 他3名 :
慢性腎臓病におけるFGF23産生亢進の分子機能解析,
第16回日本病態栄養学会年次学術集会, 2013年1月. 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一 :
肝臓切除に起因する低リン血漿発症機構の解明,
第16回日本病態栄養学会学術集会, 2013年1月. 野村憲吾, 辰巳佐和子, 木戸慎介, 瀬川博子, 宮本賢一, 他2名 :
腎臓切除後の低リン血症発症機構の解明,
第45回日本栄養食糧学会中国・四国支部大会, 2012年11月. 辰巳佐和子, 釜谷達哉, 野村憲吾, 藤田みゆき, 木戸慎介, 瀬川博子, 宮本賢一 :
骨細胞死滅マウスのり代謝異常について,
第31回腎と骨代謝研究会学術集会, 2012年10月. 木戸慎介, 藤原真理奈, 瀬川博子, 辰巳佐和子, 宮本賢一 :
カドミウム汚染によるリン代謝異常・骨軟化症発症機序の検討,
第30回日本骨代謝学会学術集会, 2012年7月. 大西沙織, 大井彰子, 杉野紗貴子, 森絢加, 瀬川博子, 宮本賢一 :
HHRHの原因遺伝子Na-Pi-IIcによる細胞内vacuole形成について,
第55回日本腎臓学会学術集会, 2012年6月. 瀬川博子, 宮本賢一, 大西沙織 :
リン代謝調節機構,
第55回日本腎臓学会学術総会, 2012年6月. 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一, 他2名 :
慢性腎臓病患者におけるFGF23産生亢進の分子機能解析.,
第66回日本栄養・食糧学会大会, 2012年5月. 辰巳佐和子, 瀬川博子, 宮本賢一, 他5名 :
骨細胞と腎臓を結ぶリン代謝調節機序,
第66回日本栄養・食糧学会大会, 2012年5月. 向井朋, 瀬川博子, 木戸慎介, 辰巳佐和子, 宮本賢一, 他10名 :
生体内リン代謝調節機構における唾液腺の関与.,
第66回日本栄養・食糧学会大会., 2012年5月. 山本浩範, 増田真志, 香西美奈, 池田翔子, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 :
レチノイン酸はIIb型リン酸トランスポーターNpt2b発現を抑制し小腸リン吸収を低下させる(会議録),
第66回日本栄養・食糧学会大会講演要旨集, 179, 2012年4月. 宮本賢一 :
カドミウムと低リン血症,
第82回日本衛生学会学術総会, 2012年3月. 藤原真理奈, 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一 :
カドミウム汚染によるリン代謝異常;骨軟化症発症機序およびバイオマーカーの探索,
第244回徳島医学会学術集会, 2012年2月. 宮本賢一, 向井朋, 辰巳佐和子, 木戸慎介, 瀬川博子 :
リン代謝における腸管の役割,
第15回日本病態栄養学会年次学術集会, 2012年1月. 木戸慎介, 橋本由衣, 藤原真理奈, 遠藤逸朗, 瀬川博子, 辰巳佐和子, 松本俊夫, 宮本賢一 :
糖尿病に併存する腎障害・骨障害の発症及び進展におけるFGF23の関与,
第15回日本病態栄養学会年次学術集会, 2012年1月. 向井朋, 瀬川博子, 石川康子, 大西沙織, 佐々木祥平, 桑原頌冶, 堀場直, 木戸慎介, 福島直, 宮本賢一 :
ナトリウム依存性リン酸トランスポーターNpt2bの新たな生理機能の解析,
第15回日本病態栄養学会年次学術集会, 2012年1月. 藤原真理奈, 木戸慎介, 瀬川博子, 辰巳佐和子, 宮本賢一 :
カドミウム汚染によるリン代謝異常:骨軟化症発症機序の検討,
第15回日本病態栄養学会年次学術集会, 2012年1月. 釜谷達哉, 辰巳佐和子, 山口誠一, 吉見文子, 木戸慎介, 瀬川博子, 宮本賢一 :
骨細胞とリン代謝,
第15回日本病態栄養学会年次学術集会, 2012年1月. 橋本由衣, 木戸慎介, 藤原真理奈, 近藤剛史, 瀬川博子, 遠藤逸朗, 辰巳佐和子, 松本俊夫, 宮本賢一 :
糖尿病合併症発症におけるFGF23/Klothoの関与,
第44回日本栄養食糧学会中四国支部大会, 2011年11月. 向井朋, 瀬川博子, 佐々木祥平, 桑原頌冶, 宮本賢一 :
ナトリウム依存性リン酸トランスポーターNpt2bの新たな生理機能の解明,
第41回日本腎臓学会西部学術大会, 2011年9月. 大西沙織, 大井彰子, 杉野紗貴子, 木戸慎介, 辰巳佐和子, 瀬川博子, 宮本賢一 :
Hereditary hypophosphatemic rickets with hypercalciuria(HHRH)やFanconi's syndromeにおける低リン血症の分子機構解明,
第41回日本腎臓学会西部学術大会, 2011年9月. 堀江大輔, 山田歩規代, 谷村綾子, 竹谷豊, 山本浩範, 宮本賢一, 武田英二 :
Na依存性リン酸トランスポーターとezrinとの新たな相互作用,
第84回日本生化学会, 2011年9月. 辰巳佐和子, 真鍋舞, 宮本賢一 :
シナカルセト塩酸塩による代謝,
第58回日本栄養改善学会学術総会,9月10日広島国際会議場,広島, 2011年9月. 竹谷豊, 山本浩範, 奥村仙示, 宮本賢一, 武田英二 :
慢性腎臓病モデルラットにおけるリン接種制限による血管内皮機能改善効果,
第58回日本栄養改善学会学術総会, 2011年9月. 木戸慎介, 藤原真理奈, 瀬川博子, 辰巳佐和子, 宮本賢一 :
イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与,
第29回日本骨代謝学会学術集会, 2011年7月. 竹谷豊, ヴヴァンタン, 宮本賢一, 山本浩範, 武田英二 :
リン制限食はアデニン誘発性CKDモデルラットにおける血管内皮機能障害を改善する,
第29回日本骨代謝学会学術集会, 2011年7月. 山本浩範, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 :
レチノイン酸はIIb型リン酸トランスポーターNpt2b発現を抑制し小腸リン吸収を低下させる,
第29回日本骨代謝学会学術集会, 2011年7月. 山本浩範, 池田翔子, 増田真志, 香西美奈, 瀬川博子, 竹谷豊, 宮本賢一, 武田英二 :
敗血症時におけるリン代謝異常の分子メカニズムの解析,
第29回日本骨代謝学会学術集会, 2011年7月. 塩﨑雄治, 杉野紗貴子, 大井彰子, 辰巳佐和子, 伊藤美紀子, 宮本賢一 :
高カルシウム尿を伴う遺伝性低リン血症性クル病の原因遺伝子リン酸トランスポーターNPT2cの変異体解析,
第54回日本腎臓病学会学術総会, 2011年6月. 山本浩範, 増田真志, 田中更紗, 香西美奈, 竹谷豊, 宮本賢一, 武田英二 :
1-II-12 All-transレチノイン酸は小腸からのリン吸収を抑制する(一般演題要旨,日本ビタミン学会第63回大会講演要旨),
ビタミン, Vol.85, No.4, 218, 2011年6月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001205784275840

(CiNii: 1390001205784275840) 瀬川博子, 古谷順也, 桑原頌冶, 辰巳佐和子, 木戸慎介, 宮本賢一 :
慢性腎臓病における食事リンによる腸管ペプチドトランスポーター調節,
第65回日本栄養・食糧学会大会, 2011年5月. 木戸慎介, 藤原真理奈, 中川航司, 瀬川博子, 辰巳佐和子, 宮本賢一 :
イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与,
第65回日本・栄養食糧学会大会, 2011年5月. 辰巳佐和子, 菊井聡子, 野村憲吾, 斉藤友紀子, 塩﨑雄治, 山口誠一, 木戸慎介, 瀬川博子, 宮本賢一 :
リン代謝におけるカルシウム受容体の役割,
第65回日本栄養・食糧学会大会, 2011年5月. 中橋乙起, 山本浩範, 田中更沙, 向原理恵, 池田翔子, 橋本脩平, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
リン制限食によるFibroblast growth factor 15遺伝子発現調節機構,
第65回日本栄養・食糧学会大会, 2011年5月. 山本浩範, 増田真志, 香西美奈, 中橋乙起, 池田翔子, 竹谷豊, 瀬川博子, 宮本賢一, 武田英二 :
レチノイン酸受容体RAR/RXRを介したナトリウム依存性リン酸輸送担体遺伝子の発現調節機構,
第65回日本栄養・食糧学会大会, 2011年5月. 瀬川博子, 古谷順也, 菅野三喜男, 坂内堅二, 大和英之, 宮本賢一 :
蛋白源に含まれるリンの有する作用:FGF23との関係,
第22回日本腎性骨症研究会, 2011年2月. 宮本賢一 :
慢性腎臓病におけるリントランスポーターの役割,
第4回革新的特色研究シンポジウム, 2011年1月. 大井彰子, 瀬川博子, 花房悦世, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 :
高リン血症治療薬の分子標的Npt2bノックアウトマウスの解析,
第14回日本病態栄養学会年次学術集会, 2011年1月. 坂田雅映, 木戸慎介, 橋本由衣, 辰巳佐和子, 瀬川博子, 松本俊夫, 宮本賢一 :
FGF23/Klothoを介した新たな腎尿細管リン・カルシウム代謝調節機構の解明,
第14回日本病態栄養学会年次学術集会, 2011年1月. 山本浩範, 香西美奈, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
甲状腺疾患におけるビタミンD代謝異常の分子メカニズムの解明,
第28回小児代謝性骨疾患研究会, 2010年12月. 宮本賢一 :
低リン血症くる病の理解に向けて-生後発達に伴う尿細管リン再吸収障害-,
第28回小児代謝性骨疾患研究会, 2010年12月. 藤原真理奈, 木戸慎介, 坂田雅映, 荒波史, 瀬川博子, 辰巳佐和子, 宮本賢一 :
イタイイタイ病に見られる骨障害の発症・進展におけるFGF23の関与,
第43回日本栄養・食糧学会中国四国支部大会, 2010年11月. 中橋乙起, 山本浩範, 田中更紗, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
リン制限及び活性型ビタミンDによるFibroblast growth factor15遺伝子発現調節,
第43回日本栄養・食糧学会中国四国支部大会, 2010年11月. 宮本賢一, 木戸慎介 :
不動性骨粗鬆症の予防に有効な機能性食品の探索,
第6回機能性宇宙食研究会, 2010年11月. 山口誠一, 辰巳佐和子, 釜谷達哉, 塩崎雄治, 野村憲吾, 斎藤友紀子, 木戸慎介, 宮本賢一 :
リン代謝における骨細胞の役割,
第29回腎と骨代謝研究会, 2010年10月. 越智ありさ, 中尾玲子, 山智成, 上村啓太, 平坂勝也, 真板綾子, 奥村裕司, 原田晃子, 長野圭介, 片桐綾人, 河村知志, 根本尚夫, 宮本賢一, 二川健 :
抗ユビキチン化ペプチドCblin (Cbl-b inhibitor)の高機能化,
日本アミノ酸学会第4回学術大会, 2010年9月. 宮本賢一 :
リンの話題,
第33回栃木県透析医学会, 2010年9月. 山本浩範, 香西美奈, 竹谷豊, 武田英二, 宮本賢一, 加藤茂明 :
1.甲状腺疾患におけるリン・ビタミンD代謝異常の分子メカニズムの解明(第326回会議研究発表要旨,脂溶性ビタミン総合研究委員会),
ビタミン, Vol.84, No.8, 408, 2010年8月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390001205701667456

(CiNii: 1390001205701667456) 木戸慎介, 中川航司, 橋本由衣, 坂田雅映, 辰巳佐和子, 荒波史, 瀬川博子, 宮本賢一 :
イタイイタイ病に見られるCd骨症(骨軟化症)の発症・進展におけるFGF23の関与,
第28回日本骨代謝学会学術集会, 2010年7月. 山本浩範, 香西美奈, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
甲状腺ホルモン受容体β1を介したビタミンD-1α水酸化酵素(SYP27B1)遺伝子の転写抑制機構,
第28回日本骨代謝学会学術集会, 2010年7月. 宮本賢一, 花房悦世, 辰巳佐和子, 木戸慎介, 瀬川博子 :
腸管とリン代謝,
第28回日本骨代謝学会学術集会, 2010年7月. 山本浩範, 香西美奈, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
甲状腺ホルモン受容体β1を介したビタミンDー1α水酸化酵素(CYP27B1)遺伝子の転写抑制機構,
第28回日本骨代謝学会学術集会，東京，平成22年7月21日~23日, 2010年7月. 宮本賢一 :
リン酸代謝調節機序:最近の知見,
第1回骨バイオサイエンス研究会, 2010年6月. 中橋乙起, 山本浩範, 池田翔子, 田中更沙, 竹井悠一郎, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
リン代謝異常および食餌性リンによる線維芽細胞増殖因子23(FGF23)の発現変動の解析,
第62回日本ビタミン学会大会,盛岡,平成22年6月11日~12日, 2010年6月. 増田真志, 山本浩範, 香西美奈, 石黒真理子, 中橋乙起, 田中更沙, 竹谷豊, 宮本賢一, 武田英二 :
腎II型ナトリウム依存性リン酸輸送担体Npt2aを介した新規ビタミンD代謝調節機構,
第62回日本ビタミン学会大会，盛岡，平成22年6月11日~12日, 2010年6月. 橋本由衣, 木戸慎介, 中川航司, 坂田雅映, 佐々木祥平, 辰巳佐和子, 宮本賢一 :
糖尿病発症における抗老化因子Klothoの関与,
第64回日本栄養・食糧学会大会, 2010年5月. 花房悦世, 瀬川博子, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 :
小腸リン酸トランスポーターNpt2bノックアウトマウスの解析,
第64回日本栄養・食糧学会大会, 2010年5月. 中川航司, 木戸慎介, 遠藤逸郎, 坂田雅映, 橋本由衣, 佐々木祥平, 辰巳佐和子, 松本俊夫, 宮本賢一 :
糖尿病性骨症の発症機序の解明:終末糖化産物(AGEs)によるCanonical Wnt経路抑制機序の解析,
第64回日本栄養・食糧学会大会, 2010年5月. 越智ありさ, 中尾玲子, 山智成, 上村啓太, 古谷順也, 真板綾子, 奥村裕司, 原田晃子, 長野圭介, 片桐綾人, 河村知志, 根元尚夫, 宮本賢一, 二川健 :
廃用性筋委縮を防ぐ抗ユビキチン化ペプチドの開発,
第64回日本栄養・食糧学会大会, 2010年5月. 松本なつき, 逸見明博, 瀬川博子, 大西律子, 宮本賢一, 大和英之 :
生体内凍結技法による腎尿細管リントランスポーターの免疫組織解析,
第64回日本栄養・食糧学会大会, 2010年5月. 谷村綾子, 鎌田歩規代, 竹谷豊, 斎藤亮彦, 堀江大輔, 山本浩範, 宮本賢一, 武田英二 :
血清リン濃度調節に関わるナトリウム依存性リン酸トランスポーターNaPi-IIa複合体の構造と機能,
第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, 2010年5月. 竹谷豊, 首藤恵泉, 宮本賢一, 武田英二 :
生活習慣病の病態における栄養素トランスポーターの役割,
シンポジウム・第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, 2010年5月. 谷村綾子, 鎌田歩規代, 竹谷豊, 斎藤亮彦, 堀江大輔, 山本浩範, 宮本賢一, 武田英二 :
血清リン濃度調節に関わるナトリウム依存性リン酸トランスポーターNaPi-IIa複合体の構造と機能,
第64回日本栄養・食糧学会大会, 2010年5月. 中橋乙起, 山本浩範, 田中更紗, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
Fibroblast Growth Factor15遺伝子の発現に及ぼす食餌性リン及び活性型ビタミンD3の影響,
第64回日本栄養・食糧学会大会, 2010年5月. 大井彰子, 富永理恵子, 伊藤美紀子, 西山俊, 杉野紗貴子, 木戸慎介, 辰巳佐和子, 瀬川博子, 宮本賢一 :
副甲状腺(PTH)によるリン代謝調節機構の解明,
第64回日本栄養・食糧学会大会, 2010年5月. 野村憲吾, 辰巳佐和子, 菊井聡子, 斎藤友紀子, 塩崎雄治, 山口誠一, 木戸慎介, 宮本賢一 :
新規リン利尿因子の探索,
第64回日本栄養・食糧学会大会, 2010年5月. 池田翔子, 山本浩範, 増田真志, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 :
敗血症におけるリン代謝異常の分子メカニズムの解析．,
第64回日本栄養・食糧学会大会, 2010年5月. 瀬川博子, 花房悦世, 堀場直, 上田乙也, 寺社下浩一, 福島直, 宮本賢一 :
高リン血症治療の標的分子探索:腸管リントランスポーターノックアウトマウスの解析,
第64回日本栄養・食糧学会大会, 2010年5月. 斎藤友紀子, 辰巳佐和子, 野村憲吾, 菊井聡子, 山口誠一, 塩崎雄治, 金子一郎, 瀬川博子, 木戸慎介, 宮本賢一 :
リン酸輸送担体遺伝子欠損マウスの病態解析,
第64回日本栄養・食糧学会大会, 2010年5月. 金子一郎, 瀬川博子, 古谷順也, 桑原頌治, 荒波史, 富永理恵子, 花房悦世, 辰巳佐和子, 木戸慎介, 加藤茂明, 宮本賢一 :
ビタミンDによるリン代謝調節機序の解明．,
第64回日本栄養・食糧学会, 2010年5月. 池田翔子, 山本浩範, 増田真志, 中橋乙起, 竹谷豊, 宮本賢一, 武田英二 :
敗血症におけるリン代謝異常の分子メカニズムの解析,
第64回日本栄養・食糧学会大会,徳島,平成22年5月21日~23日, 2010年5月. 宮本賢一 :
無機リン酸代謝調節に関する分子栄養学的研究,
第64回日本栄養・食糧学会大会, 2010年5月. 越智ありさ, 中尾玲子, 山智成, 上村啓太, 古谷順也, 真板綾子, 奥村裕司, 原田晃子, 長野圭介, 片桐綾人, 根本尚夫, 宮本賢一, 二川健 :
廃用性筋萎縮を防ぐ抗ユビキチン化ペプチドの開発,
第64回日本栄養・食糧学会大会, 2010年5月. 山本浩範, 菊地浩子, 桑原頌治, 田中更沙, 中橋乙起, 竹谷豊, 宮本賢一, 佐々木一, 武田英二 :
腸管トランスポーターを分子標的とした腎疾患治療法の確立をめざして,
第13回日本病態栄養学会年次学術集会, 2010年1月. 竹谷豊, 中村麻子, 梨木邦剛, 谷村綾子, 山本浩範, 宮本賢一, 武田英二 :
Ezrinによるリン酸トランスポーター(NaPi-IIa)分子複合体の機能調節,
日本分子生物学会年会, Vol.28, 2005年12月. Yutaka Taketani, K. Nashiki, A. Nakamura, N. Sawada, Hironori Yamamoto, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda :
Role of ezrin in the Downregulation of Sodium-Dependent Phosphate Transporter(NaPi-IIa) in Opossum Kidney Cells,
日本生化学会大会, Vol.78, Oct. 2005. Yutaka Taketani, K. Nashiki, N. Sawada, Hironori Yamamoto, Hidekazu Arai, Ken-ichi Miyamoto and Eiji Takeda :
Role of ezrin in the parathyroid hormone-mediated downregulation of sodium-dependent phosphate transporter in opossum kidney cells,
日本細胞生物学会大会, Vol.58, Jun. 2005. 山本浩範, 木村宏子, 辻光義, 石黒真理子, 竹井悠一郎, 佐藤匡俊, 宮本賢一, 白神俊幸, 田中裕子, 新井英一, 竹谷豊, 武田英二 :
腸管ペプチド輸送担体(PepT1)を分子標的とした新たな栄養補給法の開発,
日本病態栄養学会, Vol.8, 2005年1月. 宮内章光, 高木康行, 吉本祥生, 宮本賢一, 武田英二, 杉本利嗣, 山本威久, 千原和夫, M. J. Econs, H. Jueppner :
腫瘍性骨軟化症の惹起物質についての研究(FGF23の関与),
日本骨代謝学会, Vol.19, 2001年8月. 小林くみ, 山本浩範, 谷佳子, 竹谷豊, 森田恭子, 新井英一, 宮本賢一, 武田英二 :
腎近位尿細管におけるリン再吸収調節機構の解析,
日本栄養食糧学会大会, Vol.55, 2001年5月. 宮本賢一, 新居智子, 瀬川博子, 伊藤美紀子, 竹谷豊, 武田英二, 金井好克, 遠藤仁 :
CD98を介するアミノ酸輸送と感受システムの誘導機序,
日本栄養食糧学会大会, Vol.55, 2001年5月.

研究会・報告書

塩﨑雄治, 三浦美月, 宇賀穂, 小宮蒼, 原田和, 東彩生, 小池萌, 宮本賢一, 瀬川博子 :
高リン血症予防に関与する新規リン代謝調節因子Transmembrane protein (Tmem) 174の同定,
第6回日本Uremic Toxin研究会学術集会, 2023年5月. 塩﨑雄治, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 浜口ゆき, 金子一郎, 宮本賢一, 瀬川博子 :
近位尿細管細胞分化におけるリン酸トランスポーターNaPi-IIcの役割,
第1回トランスポーター研究会関西西部会JTRAKansai2021∼トランスポーター研究の架け橋∼, 2021年10月. 金子一郎, 瀬川博子, 張哲然, 加藤茂明, 宮本賢一 :
ビタミン D が制御する小腸リン吸収機序の解明,
第3回日本CKD-MBD研究会学術集会・総会, 2019年3月. 辰巳佐和子, 金子一郎, 瀬川博子, 宮本賢一 :
骨細胞除去によるミネラル代謝への影響: 骨 - 腎臓 - 腸管連関の解析,
第3回日本CKD-MBD研究会学術集会・総会, 2019年3月. 宮本賢一 :
慢性腎臓病に伴うミネラル代謝異常:多臓器ネットワークとその破綻,
第22回日本病態栄養学会年次学術集会, 2019年1月. 宮本賢一, 木戸慎介, 辰巳佐和子, 金子一郎, 瀬川博子 :
カドミウム暴露と骨軟化症:バイオマーカーの探索,
第5回日本栄養改善学会四国支部学術総会, 2018年6月. 張哲然, 瀬川博子, 野津圭二郎, 生田かよ, 藤井公, 花崎愛, 加藤茂明, 宮本賢一 :
ビタミンDによる小腸リン吸収促進機構の解明,
第5回日本栄養改善学会四国支部学術総会, 2018年6月. 辰巳佐和子, 篠原理沙, 金子一郎, 瀬川博子, 宮本賢一 :
ミネラル代謝における骨細胞減少の効果:骨細胞-腎臓-腸管連関制御,
第72回日本栄養・食糧学会大会, 2018年5月. 瀬川博子, 宮本賢一 :
消化管リン輸送機構の役割,
日本農芸化学会2017年度大会, 2017年3月. 宮本賢一 :
リンとは何か?:食を通して考える,
吉野川市CKD医療連携カンファレンス, 2016年11月. 辰巳佐和子, 高濱和子, 小柳悟, 宮本賢一 :
Elucidation of the circadian rhythm in renal phosphate excretion(腎臓リン排泄における概日リズムの解明),
第23回日本時間生物学会学術大会, 2016年11月. 辰巳佐和子, 藤井理, 宮川淳美, 宮本賢一 :
骨と健康寿命の検討について,
第63回日本栄養改善学会., 2016年9月. 宮本賢一 :
ビタミンDと腎臓,
第2回Neo Vitamin D Workshop学術集会, 2016年8月. 宮本賢一 :
リン代謝と栄養:最新の話題,
腎と栄養を考える∼in Niigata∼, 2016年7月. 宮本賢一 :
食餌性リンの話題,
北九州CKD-MBD治療講演会, 2016年7月. 宮本賢一 :
リン代謝と栄養:最新の話題,
高リン血症治療Up To Date, 2016年6月. 宮本賢一 :
リンと食生活,
第61回日本透析医学会, 2016年6月. 宮本賢一 :
リンの代謝と各種疾患との関わり∼食品中のリンUp To Date∼,
平成28年度香川県栄養士会医療職域研修会, 2016年4月. 辰巳佐和子, 藤井理, 宮川淳美, 宮本賢一 :
骨と健康寿命の検討について,
第3回日本栄養改善学会四国支部学術総会., 2016年4月. 宮本賢一 :
リン過剰とその破綻:最近の知見,
CKDマネジメントフォーラム2016, 2016年4月. 宮本賢一 :
リン代謝と栄養:新しい展開と課題,
第18回腎と栄養代謝研究会in京都, 2015年12月. 宮本賢一 :
腎臓とリンの話題,
第8回ミューズたかつき腎セミナー, 2015年9月. 宮本賢一 :
慢性腎臓病における心血管合併症対策:ミネラル管理の側面から,
第2回腎と栄養研究会, 2015年9月. 瀬川博子, 桑原三恵子, 坂内堅二, 宮本賢一 :
慢性腎臓病における蛋白性尿毒素と心肥大の関連について,
第2回腎と栄養研究会., 2015年9月. 宮本賢一 :
リンと食事の話題,
Kidney Care Conference∼中西讃腎疾患を考える会∼, 2015年9月. 宮本賢一 :
リンと食事の話題,
第1回腎と栄養懇話会, 2015年9月. 宮本賢一 :
食餌性リンの話題,
第3回腎性抗加齢医学を考える会., 2015年7月. 宮本賢一 :
リン代謝と栄養:新しい展開と課題,
第3回日本腎不全栄養研究会学術集会・総会, 2015年7月. 宮本賢一 :
リンの話題,
第13回JSWN総会., 2015年6月. 宮本賢一 :
リン過剰とその制御破綻:最近の知見,
第5回腎不全研究会, 2014年12月. 宮本賢一 :
リン代謝と栄養:最近の知見,
第10回長時間透析研究会長時間透析と栄養, 2014年11月. 宮本賢一 :
リンと栄養:最近の知見,
第16回透析に関する勉強会., 2014年10月. 宮本賢一 :
リンバランスの調節機序:最近の知見,
腎不全特別講演会., 2014年9月. 宮本賢一 :
血中リン濃度の維持機構:多臓器連関について,
第46回臨床体液研究会, 2014年9月. 宮本賢一 :
リンの栄養管理:消化と吸収面から再考する,
愛媛県透析合併症対策講演会, 2014年9月. 宮本賢一 :
リン代謝研究における新展開,
第4回広島腎不全代謝病態懇話会, 2014年8月. 宮本賢一 :
栄養とリン:最新の知見,
第6回大分ホスレノールセミナー, 2014年7月. 辰巳佐和子, 藤井理, 宮本賢一 :
骨細胞の機能と異常,
第57回日本腎臓学会学術総会, 2014年7月. 濵田康弘, 安井苑子, 宮本賢一 :
医学部における栄養学教育の問題点と展望徳島大学医学部医科栄養学科における栄養学教育への取り組み臨床栄養学教育(ベッドサイド教育)の強化へ向けて,
静脈経腸栄養, Vol.29, No.1, 275, 2014年1月.

(キーワード): *医学大学教育

瀬川博子, 佐々木祥平, 宮本賢一 :
Klothoによるリン代謝制御と老化,
第43回日本腎臓学会西部学術大会, 2013年10月. 瀬川博子, 向井朋, 森絢加, 佐々木祥平, 宮本賢一 :
リンの吸収と排泄の生体内調節.,
第56回日本腎臓学会学術総会, 2013年5月. 瀬川博子, 佐々木祥平, 向井朋, 真鍋舞, 宮本賢一 :
近位尿細管におけるリントランスポーターNaPi2cとklothoとの関わり,
第24回日本腎性骨症研究会, 2013年1月. 宮本賢一 :
リンと栄養:各国の話題,
第15回日本腎不全看護学会学術集会・総会, 2012年12月. 宮本賢一 :
リンと栄養:最近の知見,
第四回沖縄CKD-MBD研究会, 2012年11月. 宮本賢一 :
リンと栄養:最近の知見,
神戸透析研究会, 2012年10月. 辰巳佐和子, 宮本賢一, 木戸慎介, 他3名 :
骨細胞死滅マウルのリン代謝異常について,
第31回腎と骨代謝研究会学術集会, 2012年10月. 宮本賢一 :
リンと栄養:最近の知見,
ホスレノール発売3周年記念講演会顆粒分包新発売記念講演会, 2012年10月. 瀬川博子, 木戸慎介, 宮本賢一, 辰巳佐和子, 他3名 :
リンの体内動態(腸管，腎臓における吸収と排泄機序/リン輸送体の機能作用),
Clinical Calcium, Vol.22, No.10, 13-20, 2012年10月. 宮本賢一 :
リン代謝における臓器相関,
リン代謝における臓器相関, 2012年9月. 宮本賢一 :
リンの栄養学:最近の知見,
第9回富士透析勉強会, 2012年5月. 宮本賢一 :
性腎臓病におけるリン代謝異常∼FGF23/Klothoの役割について∼,
愛媛骨代謝研究会, 2012年5月. 宮本賢一 :
慢性腎臓病におけるリンの話題,
第78回大阪透析研究会, 2012年3月. 宮本賢一 :
リンバランスとその調節,
第1回湘南電解質キャンプ, 2012年2月. 宮本賢一 :
慢性腎臓病におけるリンの管理,
徳島県病院薬剤師会学術講演会, 2012年1月. 宮本賢一 :
リン代謝の話題:新しい展開とその理解に向けて,
第14回腎と栄養代謝研究会, 2011年12月. 山口誠一, 辰巳佐和子, 釜谷達哉, 吉見文子, 木戸慎介, 瀬川博子, 宮本賢一 :
骨細胞とリン代謝,
第18回徳島骨代謝研究会, 2011年11月. 宮本賢一 :
リン代謝の新しい話題:新しい展開とその理解に向けて,
西三河CKD-MBD研究会, 2011年10月. 藤原真理奈, 木戸慎介, 荒波史, 中川航司, 瀬川博子, 辰巳佐和子, 宮本賢一 :
カドミウムによるFibroblast growth factor23(FGF23)発現調節機序の検討,
第30回腎と骨代謝研究会学術集会, 2011年10月. 野村憲吾, 辰巳佐和子, 山口誠一, 塩﨑雄治, 菅生陵馬, 木戸慎介, 瀬川博子, 宮本賢一 :
肝臓切除による低リン血症発症メカニズムの解明,
第30回腎と骨代謝研究会学術集会, 2011年10月. 宮本賢一 :
慢性腎臓病とFGF23/Klotho:最近の知見,
臓器保護と治療研究会, 2011年9月. 宮本賢一 :
リン代謝の話題:新しい展開とその理解に向けて,
20th北海道MBD研究会, 2011年9月. 宮本賢一 :
リン代謝の話題:新しい展開とその理解に向けて,
信州CKD血管障害研究会∼透析と栄養を考える∼, 2011年7月. 宮本賢一 :
リン代謝の話題:新しい展開とその理解に向けて,
ホスレノール発売2周年記念講演会, 2011年7月. 宮本賢一 :
リン調節ホルモンと臓器相関:最新の知見,
第23回Kobe Parathyroid and Bone Forum, 2011年6月. 増田真志, 山本浩範, 香西美奈, 竹井悠一郎, 中橋乙起, 池田翔子, 大谷彩子, 竹谷豊, 宮本賢一, 武田英二 :
All-transレチノイン酸による腸管リン吸収への影響とそのメカニズム,
日本農芸化学会中四国支部第29回講演会/日本ビタミン学会中国・四国地区第1回講演会合同講演会, 2011年1月. 中橋乙起, 山本浩範, 田中更沙, 増田真志, 竹谷豊, 宮本賢一, 加藤茂明, 武田英二 :
リン制限及び活性型ビタミンDによるFibroblast growth factor 15遺伝子発現調節,
第43回日本栄養・食糧学会中国・四国支部大会, 2010年11月. 宮本賢一, 辰巳佐和子, 金子一郎, 瀬川博子 :
大豆たん白質摂取による心肥大抑制効果の検討.,
大豆たん白質研究., Vol.21, 83-89, 2019年.

特許: 研究者総覧に該当データはありませんでした。
作品: 研究者総覧に該当データはありませんでした。
補助金・競争的資金: 新規リンネットワーク破綻がもたらす栄養障害の分子機序解明 (研究課題/領域番号: 20K08637 )
無機リン酸（リン）応答複合体機能の解明とリン過剰克服に向けた新戦略 (研究課題/領域番号: 17H04190 )
老化制御と食事因子：糖鎖修飾ダイエット (研究課題/領域番号: 15K12340 )
筋収縮機能を回復するミトコンドリア・リハビリテーション学 (研究課題/領域番号: 15H04960 )
脳室内リン制御による全身性リン過剰の克服 (研究課題/領域番号: 26293204 )
食事組成の科学的根拠を提示する栄養素に対するトランスセプターの同定 (研究課題/領域番号: 23650480 )
リン代謝異常を惹起する臓器相関シグナル因子の解明 (研究課題/領域番号: 23390226 )
腎不全時のカルシウム/リン比を維持し、骨に導く先導分子の同定 (研究課題/領域番号: 20590976 )
生命予後を規定する骨・血管型リンチャネルの分子制御機構 (研究課題/領域番号: 20590975 )
FGF23/klotho/リンセンサーを介したリン代謝ホルモンの同定と機能解明 (研究課題/領域番号: 20390236 )
FGF23/klothoによるミネラル代謝と寿命制御 (研究課題/領域番号: 18659251 )
リンセットポイントを規定するセンサー分子の統御機構解明 (研究課題/領域番号: 18390250 )
リン利尿因子フォスファトニン感受ペプチドASARM受容体の同定 (研究課題/領域番号: 17659256 )
無機リン酸トランスポートソームの機能制御とその破綻 (研究課題/領域番号: 17081013 )
Klotho老化学を裏付けるリン老化説構成回路(寿命ホルモン)の同定 (研究課題/領域番号: 16659225 )
リンセンサー分子を介したカルシウム・リン積制御機構の解明 (研究課題/領域番号: 16390244 )
リンセンサー分子の同定と機能解析 (研究課題/領域番号: 14657254 )
リンセンサー分子の同定と新規リンシグナルネットワーク分子統制機能の解明 (研究課題/領域番号: 14370320 )
リン代謝調節系を支配するシグナルネットワーク分子の発見と分子統制機能の解明 (研究課題/領域番号: 12470211 )
DNAマイクロチップを用いた疾患別多次元遺伝子多型解析法の開発 (研究課題/領域番号: 11557202 )
慢性腎不全時における新規リン調節ホルモン(フォスファトニン)活性化の分子機構 (研究課題/領域番号: 10670999 )
新規カルシウム・リン代謝調節ホルモン(フォスファトニン)の測定法の開発 (研究課題/領域番号: 10557096 )
一回の膜貫通領域をもつアミノ酸輸送担体の分子構造および機能解析 (研究課題/領域番号: 09257233 )
リン調節蛋白(Phosphatonin及びPEX)異常と低リン血症発症の分子機構 (研究課題/領域番号: 08671288 )
一回の膜貫通域をもつアミノ酸輸送担体の分子構造と機能解析 (研究課題/領域番号: 08268236 )
ラジオアイソトープを用いない血中1,25-ジヒドロキシビタミンD濃度測定法の開発 (研究課題/領域番号: 07557321 )
一回の膜貫通領域をもつアミノ酸輸送担体の分子構造および機能解析 (研究課題/領域番号: 07276227 )
ビタミンD受容体のゲノム遺伝子解析とビタミンD受容体障害の簡易検出法の確立 (研究課題/領域番号: 06670800 )
ヒト低リン血性クル病の原因である腎Na/リン輸送担体遺伝子のクローニング (研究課題/領域番号: 05670145 )
ビタミンD受容体障害の分子遺伝学的解析とビタミンD作用の発現調節に関する研究 (研究課題/領域番号: 04670601 )
研究者番号（70174208）による検索

その他: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年4月26日更新

専門分野・研究分野: 保健学 (Health Studies)
所属学会・所属協会: 日本病態栄養学会
日本栄養・食糧学会
日本生化学学会
日本腎学会
委員歴・役員歴: 日本病態栄養学会 (幹事)
日本栄養・食糧学会 (評議員)
日本生化学学会 (評議員)
日本腎学会 (学術評議員)
受賞: 2010年5月, 学会賞・奨励賞 (社団法人日本栄養・食糧学会)
活動: 研究者総覧に該当データはありませんでした。

リサーチマップで最新データを確認するＪグローバルで最新データを確認する

2024年4月21日更新

2024年4月20日更新

Ｊグローバル

Jグローバル最終確認日: 2024/4/20 01:30
氏名（漢字）: 宮本賢一
氏名（フリガナ）: ミヤモトケンイチ
氏名（英字）: ken'ichi miyamoto
所属機関: 龍谷大学特任教授

リサーチマップ

researchmap最終確認日

2024/4/21 01:54

氏名（漢字）

宮本賢一

氏名（フリガナ）

ミヤモトケンイチ

氏名（英字）

ken'ichi miyamoto

プロフィール

昭和５４年３月徳島大学医学部栄養学科卒業（管理栄養士）
昭和５９年４月徳島大学助手医学部（病態栄養学講座）
平成元年１月徳島大学大学院栄養学研究科博士後期課程修了
１月保健学博士学位授与（徳島大学甲栄５６号）
１月米国シカゴ大学生命科学研究所分子生物学部門
学術研究員
平成４年４月徳島大学大学院講師医学部
平成６年４月徳島大学助教授医学部（病態栄養学講座）
平成１１年10月徳島大学教授医学部（栄養化学講座）
平成１６年 4月徳島大学教授大学院ヘルスバイオサイエンス研究部
（分子栄養学分野）

令和２年４月龍谷大学農学部食品栄養学科（病態栄養研究室）

登録日時

2019/5/21 11:07

更新日時

2024/1/31 08:43

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2553818003

所属

龍谷大学

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農学部食品栄養学科

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特任教授

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保健学

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徳島大学

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ＫＡＫＥＮで最新データを確認する

2024年4月20日更新

研究者番号: 70174208

所属（現在）: 2024/4/1 : 龍谷大学, 農学部, 教授

所属（過去の研究課題 情報に基づく）*注記: 2022/4/1 : 龍谷大学, 農学部, 教授
2021/4/1 : 龍谷大学, 農学部, 特任教授
2020/4/1 : 龍谷大学, 農学部, 教授
2018/4/1 – 2019/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 教授
2016/4/1 – 2017/4/1 : 徳島大学, 大学院医歯薬学研究部(医学系), 教授
2015/4/1 – 2016/4/1 : 徳島大学, 大学院医歯薬学研究部, 教授
2011/4/1 – 2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 教授
2004/4/1 – 2012/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授
2005/4/1 – 2006/4/1 : 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授
1999/4/1 – 2003/4/1 : 徳島大学, 医学部, 教授
1994/4/1 – 1998/4/1 : 徳島大学, 医学部, 助教授
1992/4/1 – 1993/4/1 : 徳島大学, 医学部, 助手

審査区分/研究分野

研究代表者

医学 / 内科 / 腎臓内科学
生物系 / 医歯薬学 / 内科系臨床医学 / 腎臓内科学
総合・新領域系 / 総合領域 / 生活科学 / 食生活学
医学 / 生理 / 病態医化学
医学 / 医学一般 / 人類遺伝学
総合系 / 複合領域 / 生活科学 / 食生活学
生物系
小区分53040:腎臓内科学関連

研究代表者以外

医学 / 内科 / 小児科学
生物系 / 医歯薬学 / 内科系臨床医学 / 腎臓内科学
医学 / 医学一般 / 病態検査学
医学 / 内科 / 腎臓内科学
生物系 / 医歯薬学 / 外科系臨床医学 / 整形外科学

キーワード

研究代表者

アミノ酸 / 輸送担体 / シスチン尿症 / 遺伝子解析 / Amino Acid / Transporter / cystinuria / Phosphate / sensor / Kidney / FGF23 / phosphate / transporter / kidney / 無機リン酸 / 腎臓 / ナトリウム依存性 / 輸送体 / リン利尿因子Inorganic phosphate / Sodium-dependent / phosphaturic factor / 膜輸送 / 分子認識 / 賢臓 / リン酸 / fibroblast growth factor 23 / マイクロドメイン / リン / 腎尿細管 / トランスポーター / エンドサイトーシス / 脂質マイクロドメイン / PTH / Ezrin / フォスファトニン / 受容体 / 腎 / カルシウム / klotho / 老化 / ビタミンD / 副甲状腺ホルモン / 骨 / 低リン血症 / クル病 / 腸管 / クロライド / ノックアウトマウス / 肝臓 / グルコース / 腎総 / リン利尿 / 繊維芽細胞増殖因子２３ (FGF23) / 骨細胞 / Klotho / 慢性腎臓病 / トランスセプター / 破骨細胞 / 栄養 / トランセプター / ミネラル / リンセンサー / 食事 / 唾液 / リン代謝 / 脳室 / 唾液腺 / 低リン血性クル病 / 刷子縁膜 / リン輸送担体 / アフリカツメガエル / アンチセンスオリゴヌクレチオチド / 低リン血症クル病 / アフリツメガエル / アンチセンスオリゴヌクレオチド / クローニング / Hypophosphatemia / Renal proximal tubule / Brush border membrane / Phosphate transporter / Xenopus oocytes / Antisense oligonucleotide / 遺伝子異常 / マウス / Phosphatonin / Gene Mutation / Mouse / スタニオカルシン / PEX / Stanniocalcin / Hyphophosphatemia / ビタミンD受容体 / DNA analysis / 骨粗鬆症 / 遺伝子多型 / 骨密度 / DNA / マイクロチップ / FRET / vitamin D receptor / osteoporosis / polymorphism / calcium absorption / phosphate sensor / phosphate transporter / Hyperphosphatemia / PHEX / 腎機能 / キイロショウジョウバエ / プロテアーゼ / 液性因子 / 骨代謝 / Phosphate sensor / phosphatonin / receptor / Brain / HHRH / hypophosphatemia / mineralization / rickets / 寿命 / 糖鎖 / 亜鉛 / ミトコンドリア / リン輸送体 / 遺伝子欠損マウス / 尿細管 / 栄養障害 / 近位尿細管 / ATP / NAD / エネルギー / 筋肉

研究代表者以外

ビタミンD / ビタミンD受容体 / ゲノム遺伝子構造 / ビタミンD依存性くる病II型 / 人工透析 / リン / カルシウム / 異所性石灰化 / 破骨細胞 / リン酸トランスポーター / 骨細胞 / 腎臓 / 慢性腎臓病 / 腎不全 / 腸管 / 骨 / 腎臟 / オステオカルシン / 転写調節 / ビタミンD依存性くる病2型 / Vitamin D / Vitamin D receptor / Osteocalcin / Transcriptional regulation / Vitamin D dependent rickets type II / エンザイムレセプターアッセイ / 活性型ビタミンD / 1,25-ジヒドロキシビタミンD / 骨粗鬆症 / 臨床検査 / enzyme receptor assay / vitamin D receptor / 1,25-dihydroxyvitamin D / フォスファトニン / Na依存性リン輸送担体 / スタニオカルシン2 / 遺伝性低リン血症 / 腫瘍性低リン血性骨軟化症 / phosphatonin / sodium-dependent phosphate transporter / stanniocalcin 2 / hereditary hypophosphatemia / 筋萎縮 / ミトコンドリア / 酸化ストレス / 抗酸化栄養素 / ユビキチンリガーゼCbl-b / 転写因子Egr / 筋拘縮 / 分子リハビリテーション / 遅筋の速筋化 / Egr / アコニターゼ / 国際宇宙ステーション / メカノセンシング / ミトコンドリア酵素 / オルガネラ相関 / Mitofusin-2 / メカノセンサー / カルシウムシグナリング

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2020年6月23日

徳島大学宇宙食品産業・栄養学研究センターによる近未来型宇宙食糧ソリューション

二川健出口祥啓河合慶親宮本賢一酒井徹濵田康弘中尾玲子向井理恵高橋章宮脇克行粟飯原睦美岸本幸治原口雅宣阪上浩竹谷豊木内陽介芥川正武榎本崇宏

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宮本 賢一

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宮本賢一