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塩﨑雄治

徳島大学

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2025年5月9日更新

職名: 助教
電話: 088-633-7082
電子メール: shiozaki.yuji@tokushima-u.ac.jp
学歴: 2015/7: 徳島大学大学院栄養生命科学教育部博士後期課程修了
学位: 博士(栄養学) (徳島大学) (2015年7月)
職歴・経歴: 2015/9: Post-doctoral fellow, University of Colorado Anschutz Medical Campus, Division of Renal Diseases and Hypertension (~2021.03)

専門分野・研究分野: 研究者総覧に該当データはありませんでした。

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2025年5月9日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。
担当経験のある授業科目: ライフステージ栄養学 (学部)
公衆衛生学実習 (学部)
基礎栄養学実習 (学部)
栄養生物学 (学部)
栄養英語 (学部)
生化学・分子生物学 (学部)
生化学実験 (学部)
生物有機化学 (学部)
指導経験: 1人 (修士), 1人 (博士)

研究者総覧で最新データを確認する

2025年5月9日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。

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著書

Masashi Masuda, Yuji Shiozaki and Makoto Miyazaki :
Chapter 10 - Lipotoxicity in the pathogenesis of chronic kidney disease complications,
Academic Press, Aug. 2023.

(出版サイトへのリンク): ● Publication site (DOI): 10.1016/C2021-0-02221-5
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1016/C2021-0-02221-5

(DOI: 10.1016/C2021-0-02221-5) Masashi Masuda, Yuji Shiozaki and Makoto Miyazaki :
Lipotoxicity in the pathogenesis of chronic kidney disease complications,
Jan. 2023.

(キーワード): Autophagy / Chronic kidney disease / Endoplasmic reticulum stress / Glycerol-3-phosphate acyltransferase / Lipotoxicity / Saturated fatty acids / Stearoyl-CoA desaturase (SCD) / Vascular calcification
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/B978-0-323-95582-9.00001-2
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85207214366

(DOI: 10.1016/B978-0-323-95582-9.00001-2, Elsevier: Scopus) 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. Yuji Shiozaki, L. Audrey Keenan and Makoto Miyazaki :
Role of bile acid receptors in the regulation of cardiovascular diseases,
Jan. 2020.

(キーワード): Atherosclerosis / Bile acids / FXR / TGR5 / Vascular calcification
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/B978-0-12-819404-1.00020-8
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85124853356

(DOI: 10.1016/B978-0-12-819404-1.00020-8, Elsevier: Scopus)

論文

Minori Uga, Ichiro Kaneko, Yuji Shiozaki, Megumi Koike, Naoko Tsugawa, W. Peter Jurutka, Ken-ichi Miyamoto and Hiroko Segawa :
The Role of Intestinal Cytochrome P450s in Vitamin D Metabolism,
Biomolecules, Vol.14, No.6, 2024.

(要約): Vitamin D hydroxylation in the liver/kidney results in conversion to its physiologically active form of 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃]. 1,25(OH)₂D₃ controls gene expression through the nuclear vitamin D receptor (VDR) mainly expressed in intestinal epithelial cells. Cytochrome P450 (CYP) 24A1 is a catabolic enzyme expressed in the kidneys. Interestingly, a recently identified mutation in another CYP enzyme, CYP3A4 (gain-of-function), caused type III vitamin D-dependent rickets. CYP3A are also expressed in the intestine, but their hydroxylation activities towards vitamin D substrates are unknown. We evaluated CYP3A or CYP24A1 activities on vitamin D action in cultured cells. In addition, we examined the expression level and regulation of CYP enzymes in intestines from mice. The expression of CYP3A or CYP24A1 significantly reduced 1,25(OH)₂D₃-VDRE activity. Moreover, in mice, Cyp24a1 mRNA was significantly induced by 1,25(OH)₂D₃ in the intestine, but a mature form (approximately 55 kDa protein) was also expressed in mitochondria and induced by 1,25(OH)₂D₃, and this mitochondrial enzyme appears to hydroxylate 25OHD₃ to 24,25(OH)₂D₃. Thus, CYP3A or CYP24A1 could locally attenuate 25OHD₃ or 1,25(OH)₂D₃ action, and we suggest the small intestine is both a vitamin D target tissue, as well as a newly recognized vitamin D-metabolizing tissue.
(キーワード): 1,25(OH) D 2 3 / 25OHD 3 / CYP24A1 / CYP3A / vitamin D
(徳島大学機関リポジトリ): ● Metadata: 2013209
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/biom14060717
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38927120; ● Summary page in Scopus @ Elsevier: 2-s2.0-85197170518

(徳島大学機関リポジトリ: 2013209, DOI: 10.3390/biom14060717, PubMed: 38927120, Elsevier: Scopus) Shinobu Miyazaki-Anzai, Masashi Masuda, Audrey L Keenan, Yuji Shiozaki, Jose G Miranda and Makoto Miyazaki :
Activation of the IKK2/NF-κB pathway in VSMCs inhibits calcified vascular stiffness in CKD,
JCI Insight, Vol.9, No.7, 12:e174977, 2024.

(要約): IKK2/NF-κB pathway-mediated inflammation in vascular smooth muscle cells (VSMCs) has been proposed to be an etiologic factor in medial calcification and stiffness. However, the role of the IKK2/NF-κB pathway in medial calcification remains to be elucidated. In this study, we found that chronic kidney disease (CKD) induces inflammatory pathways through the local activation of the IKK2/NF-κB pathway in VMSCs associated with calcified vascular stiffness. Despite reducing the expression of inflammatory mediators, complete inhibition of the IKK2/NF-κB pathway in vitro and in vivo unexpectedly exacerbated vascular mineralization and stiffness. In contrast, activation of NF-κB by SMC-specific IκBα deficiency attenuated calcified vascular stiffness in CKD. Inhibition of the IKK2/NF-κB pathway induced cell death of VSMCs by reducing anti-cell death gene expression, whereas activation of NF-κB reduced CKD-dependent vascular cell death. In addition, increased calcification of extracellular vesicles through the inhibition of the IKK2/NF-κB pathway induced mineralization of VSMCs, which was significantly reduced by blocking cell death in vitro and in vivo. This study reveals that activation of the IKK2/NF-κB pathway in VSMCs plays a protective role in CKD-dependent calcified vascular stiffness by reducing the release of apoptotic calcifying extracellular vesicles.
(キーワード): Humans / NF-kappa B / Signal Transduction / Vascular Stiffness / Muscle, Smooth, Vascular / Renal Insufficiency, Chronic
(徳島大学機関リポジトリ): ● Metadata: 2011876
(出版サイトへのリンク): ● Publication site (DOI): 10.1172/jci.insight.174977
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38470493; ● Search Scopus @ Elsevier (PMID): 38470493; ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.174977

(徳島大学機関リポジトリ: 2011876, DOI: 10.1172/jci.insight.174977, PubMed: 38470493) 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, Vol.74, No.3, 221-229, 2024.

(キーワード): growth hormone / α-klotho / kidney / CKD / GH-resistant
(徳島大学機関リポジトリ): ● Metadata: 2011875
(出版サイトへのリンク): ● Publication site (DOI): 10.3164/jcbn.23-127
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390581468909331072; ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-127

(徳島大学機関リポジトリ: 2011875, DOI: 10.3164/jcbn.23-127, CiNii: 1390581468909331072) Kazuya Tanifuji, Yuji Shiozaki, Megumi Koike, Minori Uga, Aoi Komiya, Mizuki Miura, Ayami Higashi, Takaaki Shimohata, Akira Takahashi, Noriko Ishizuka, Hisayoshi Hayashi, 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: 2010979
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85158898733

(徳島大学機関リポジトリ: 2010979, DOI: 10.2152/jmi.70.260, PubMed: 37164731, Elsevier: Scopus) 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, 6353, 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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85128265225

(DOI: 10.1038/s41598-022-10409-3, PubMed: 35428804, Elsevier: Scopus) 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: 2009990
(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: 2009990, DOI: 10.2152/jmi.69.173, PubMed: 36244766, Elsevier: Scopus) Yuji Shiozaki, Shinobu Miyazaki-Anzai, Kayo Okamura, L. Audrey Keenan, Masashi Masuda and Makoto Miyazaki :
GPAT4-Generated Saturated LPAs Induce Lipotoxicity through Inhibition of Autophagy by Abnormal Formation of Omegasomes,
iScience, Vol.23, No.5, 2020.

(キーワード): Cell Biology / Lipidomics / Molecular Biology
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.isci.2020.101105
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85084367453

(DOI: 10.1016/j.isci.2020.101105, Elsevier: Scopus) Shohei Kohno, Yuji Shiozaki, L. Audrey Keenan, Shinobu Miyazaki-Anzai and Makoto Miyazaki :
An N-terminal-truncated isoform of FAM134B (FAM134B-2) regulates starvation-induced hepatic selective ER-phagy,
Life Science Alliance, Vol.2, No.3, 2019.

(要約): Autophagy is a conserved system that adapts to nutrient starvation, after which proteins and organelles are degraded to recycle amino acids in response to starvation. Recently, the ER was added to the list of targets of autophagic degradation. Autophagic degradation pathways of bulk ER and the specific proteins sorted through the ER are considered key mechanisms in maintaining ER homeostasis. Four ER-resident proteins (FAM134B, CCPG1, SEC62, and RTN3) have been identified as ER-resident cargo receptors, which contain LC3-interacting regions. In this study, we identified an N-terminal-truncated isoform of FAM134B (FAM134B-2) that contributes to starvation-induced ER-related autophagy. Hepatic FAM134B-2 but not full-length FAM134B (FAM134B-1) is expressed in a fed state. Starvation drastically induces FAM134B-2 but no other ER-resident cargo receptors through transcriptional activation by C/EBPβ. C/EBPβ overexpression increases FAM134B-2 recruitment into autophagosomes and lysosomal degradation. FAM134B-2 regulates lysosomal degradation of ER-retained secretory proteins such as ApoCIII. This study demonstrates that the C/EBPβ-FAM134B-2 axis regulates starvation-induced selective ER-phagy.
(キーワード): Amino Acid Sequence / Animals / Autophagy / CCAAT-Enhancer-Binding Protein-beta / Endoplasmic Reticulum / Gene Expression Profiling / Gene Expression Regulation / Humans / Intracellular Signaling Peptides and Proteins / Liver / Lysosomes / Membrane Proteins / Mice / Protein Isoforms / Starvation / Transcription, Genetic
(出版サイトへのリンク): ● Publication site (DOI): 10.26508/lsa.201900340
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31101736; ● Summary page in Scopus @ Elsevier: 2-s2.0-85067701927

(DOI: 10.26508/lsa.201900340, PubMed: 31101736, 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.

(要約): Injection of parathyroid hormone (PTH) rapidly stimulates renal Pi excretion, in part by downregulating NaPi-IIa (Npt2a/SLC34A1) and NaPi-IIc (Npt2c/SLC34A3) transporters. The mechanisms underlying the effects of PTH on NaPi-IIc are not fully elucidated. We analyzed the effect of PTH on inorganic phosphate (Pi) reabsorption in Npt2a^-/- mice to eliminate the influence of Npt2a on renal Pi reabsorption. In opossum kidney (OK) cells and Xenopus oocytes, we investigated the effect of NaPi-IIc transporter phosphorylation. Studies of mice with mutations of NaPi-IIc protein in which serine and threonine were replaced with either alanine (A), which prevents phosphorylation, or aspartic acid (D), which mimics the charged state of phosphorylated NaPi-IIc, were also performed to evaluate the involvement of phosphorylation in the regulation of transport function. The Npt2a^-/- experiments showed that PTH administration rapidly inactivated NaPi-IIc function in the apical membrane of proximal tubular cells. Analysis of mutant proteins (S71, S138, T151, S174, T583) at putative protein kinase C sites, revealed that S138 markedly suppressed the function and cellular expression of mouse NaPi-IIc in Xenopus oocytes and OK cells. In addition, 138D had a short half-life compared with wild-type protein. The present study suggests that acute regulation of NaPi-IIc protein by PTH is involved in the inactivation of Na⁺-dependent Pi cotransporter activity and that phosphorylation of the transporter is involved in the rapid modification.
(キーワード): Animals / Cell Line / Female / Kidney Tubules, Proximal / Male / Mice, Knockout / Opossums / Parathyroid Hormone / Peptide Fragments / Phosphates / Phosphorylation / Protein Kinase C / Protein Processing, Post-Translational / Protein Stability / Renal Reabsorption / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIc / Time Factors / Xenopus
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85063161913

(DOI: 10.1007/s10157-019-01725-6, PubMed: 30895530, Elsevier: Scopus) 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.

(要約): Inorganic phosphate (Pi) secretion from the salivary glands and dietary Pi are key Pi sources. The regulatory mechanisms of Pi homeostasis in the salivary glands are unknown. We investigated how salivary Pi concentrations are regulated by dietary Pi in mouse models. Dietary manipulation significantly changed the levels of Npt2b protein in the salivary gland ductal cells. In addition, rapid feeding on a high-Pi diet increased the saliva Pi concentrations and led to rapid endocytosis of Npt2b in the apical membranes of the duct cells. Global Npt2b^± mice exhibited increased salivary Pi concentrations and intestine-specific deletion of Npt2b after high Pi loading increased the salivary Pi concentrations. These findings indicate that Npt2b levels in the salivary glands affect the salivary Pi concentration and are regulated by dietary Pi. Intestinal Npt2b levels might also affect salivary Pi concentrations as well as renal Pi excretion. These findings suggest Pi is endogenously recycled by salivary Pi secretion, intestinal Pi absorption, and renal Pi excretion.
(キーワード): Adaptation, Physiological / Animals / Intestinal Absorption / Intestinal Mucosa / Kidney / Male / Mice / Mice, Inbred C57BL / Phosphates / Phosphorus, Dietary / Renal Elimination / Salivary Glands / Sodium-Phosphate Cotransporter Proteins, Type IIb
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85058064050

(DOI: 10.1007/s00424-018-2242-9, PubMed: 30523405, Elsevier: Scopus) 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.

(要約): The role of Na⁺-dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na⁺-dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Another Na⁺-dependent type II transporter, (NPT2A/Npt2a/NaPi-IIa), is also important for renal Pi reabsorption in humans. In mice, Npt2c deletion does not lead to hypophosphatemia and rickets because Npt2a compensates for the impaired Pi reabsorption. To clarify the differences between mouse and human, we investigated the relation between NaPi-IIa and NaPi-IIc functions in opossum kidney (OK) cells. We cloned NaPi-IIc from OK cells and created opossum NaPi-IIc (oNaPi-IIc) antibodies. We used oNaPi-IIc small interference (si)RNA and investigated the role of NaPi-IIc in Pi transport in OK cells. We cloned opossum kidney NaPi-IIc cDNAs encoding 622 amino acid proteins (variant1) and examined their pH- and sodium-dependency. The antibodies reacted specifically with 75-kDa and 150-kDa protein bands, and the siRNA of NaPi-IIc markedly suppressed endogenous oNaPi-IIc in OK cells. Treatment with siRNA significantly suppressed the expression of NaPi-4 (NaPi-IIa) protein and mRNA. oNaPi-IIc siRNA also suppressed Na⁺/H⁺ exchanger regulatory factor 1 expression in OK cells. These findings suggest that NaPi-IIc is important for the expression of NaPi-IIa (NaPi-4) protein in OK cells. Suppression of Npt2c may downregulate Npt2a function in HHRH patients.
(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: 2006459
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85062155521

(徳島大学機関リポジトリ: 2006459, DOI: 10.1007/s10157-018-1653-4, PubMed: 30317447, Elsevier: Scopus) 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.

(要約): Hyperphosphatemia is a serious complication of late-stage chronic kidney disease (CKD). Intestinal inorganic phosphate (Pi) handling plays an important role in Pi homeostasis in CKD. We investigated whether intestinal alkaline phosphatase 3 (Akp3), the enzyme that hydrolyzes dietary Pi compounds, is a target for the treatment of hyperphosphatemia in CKD. We investigated Pi homeostasis in Akp3 knockout mice (Akp3-/-). We also studied the progression of renal failure in an Akp3-/- mouse adenine treated renal failure model. Plasma, fecal, and urinary Pi and Ca concentration were measured with commercially available kit, and plasma fibroblast growth factor 23, parathyroid hormone, and 1,25(OH)2D3 concentration were measured with ELISA. Brush border membrane vesicles were prepared from mouse intestine using the Ca2+ precipitation method and used for Pi transport activity and alkaline phosphatase activity. In vivo intestinal Pi absorption was measured with oral 32P administration. Akp3-/- mice exhibited reduced intestinal type II sodium-dependent Pi transporter (Npt2b) protein levels and Na-dependent Pi co-transport activity. In addition, plasma active vitamin D levels were significantly increased in Akp3-/- mice compared with wild-type animals. In the adenine-induced renal failure model, Akp3 gene deletion suppressed hyperphosphatemia. The present findings indicate that intestinal Akp3 deletion affects Na+-dependent Pi transport in the small intestine. In the adenine-induced renal failure model, Akp3 is predicted to be a factor contributing to suppression of the plasma Pi concentration.
(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: 2006030
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-85053761468

(徳島大学機関リポジトリ: 2006030, DOI: 10.1159/000493379, PubMed: 30212831, Elsevier: Scopus) Yuji Shiozaki, Kayo Okamura, Shohei Kohno, L. Audrey Keenan, Kristina Williams, Xiaoyun Zhao, S. Wallace Chick, Shinobu Miyazaki-Anzai and Makoto Miyazaki :
The CDK9 - cyclin T1 complex mediates saturated fatty acid-induced vascular calcification by inducing expression of the transcription factor CHOP,
The Journal of Biological Chemistry, Vol.293, No.44, 17008-17020, 2018.

(要約): Vascular calcification (or mineralization) is a common complication of chronic kidney disease (CKD) and is closely associated with increased mortality and morbidity rates. We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification. Here, using mouse models of CKD, we 1) studied the contribution of the proapoptotic transcription factor CCAAT enhancer-binding protein homologous protein (CHOP) to CKD-dependent medial calcification, and 2) we identified an additional regulator of ER stress-mediated CHOP expression. Transgenic mice having smooth muscle cell (SMC)-specific CHOP expression developed severe vascular apoptosis and medial calcification under CKD. Screening of a protein kinase inhibitor library identified 16 compounds, including seven cyclin-dependent kinase (CDK) inhibitors, that significantly suppressed CHOP induction during ER stress. Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not. Cyclin T1 knockout inhibited SFA-mediated induction of CHOP and mineralization, whereas deletion of cyclin T2 and cyclin K promoted CHOP expression levels and mineralization. Of note, the CDK9-cyclin T1 complex directly phosphorylated and activated ATF4. These results demonstrate that the CDK9-cyclin T1 and CDK9-cyclin T2/K complexes have opposing roles in CHOP expression and CKD-induced vascular calcification. They further reveal that the CDK9-cyclin T1 complex mediates vascular calcification through CHOP induction and phosphorylation-mediated ATF4 activation.
(キーワード): Activating Transcription Factor 4 / Animals / Cyclin T / Cyclin-Dependent Kinase 9 / Endoplasmic Reticulum Stress / Fatty Acids / Humans / Male / Mice / Mice, Inbred DBA / Mice, Transgenic / Myocytes, Smooth Muscle / Phosphorylation / Protein Binding / Renal Insufficiency, Chronic / Transcription Factor CHOP / Vascular Calcification
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.RA118.004706
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30209133; ● Summary page in Scopus @ Elsevier: 2-s2.0-85056043599

(DOI: 10.1074/jbc.RA118.004706, PubMed: 30209133, Elsevier: Scopus) Shinobu Miyazaki-Anzai, Masashi Masuda, Shohei Kohno, Moshe Levi, Yuji Shiozaki, L. Audrey Keenan and Makoto Miyazaki :
Simultaneous inhibition of FXR and TGR5 exacerbates atherosclerotic formation,
Journal of Lipid Research, Vol.59, No.9, 1709-1713, 2018.

(要約): Simultaneous activation of bile acid receptors farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (TGR5) by INT-767 significantly reduces atherosclerotic formation. In this study, we investigated the effect of simultaneous inactivation of these bile acid receptors in atherosclerosis and which bile acid receptor mediates the anti-atherogenic effect of INT-767. To investigate the role of simultaneous inactivation of FXR and TGR5 in vivo, we generated LDL receptor knockout (LDLR) KO mice with FXR and TGR5 dual deficiency, which exhibited severe atherosclerosis and aortic inflammation through nuclear factor κΒ activation. The lipid-lowering effects of INT-767 were completely blocked by FXR single deficiency but not TGR5 single deficiency. INT-767 was able to block atherosclerotic formation and decrease levels of aortic cytokines and chemokines in LDLR KO mice under either FXR or TGR5 single deficiency. Dual deficiency of FXR and TGR5 completely blocked the anti-atherogenic and anti-inflammatory effects of INT-767 in LDLR KO mice. We demonstrated that 1) FXR and TGR5 dual deficiency exacerbated the development of atherosclerosis and 2) the anti-atherogenic effect of INT-767 requires the anti-inflammatory effect but not the lipid-lowering effect through the simultaneous activation of FXR and TGR5. Our results indicate that dual activation of FXR and TGR5 is a promising strategy for treating atherosclerosis.
(キーワード): Animals / Atherosclerosis / Bile Acids and Salts / Gene Knockout Techniques / Male / Mice / Mice, Inbred C57BL / Receptors, Cytoplasmic and Nuclear / Receptors, G-Protein-Coupled / Receptors, LDL
(出版サイトへのリンク): ● Publication site (DOI): 10.1194/jlr.M087239
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29976576; ● Summary page in Scopus @ Elsevier: 2-s2.0-85052728921

(DOI: 10.1194/jlr.M087239, PubMed: 29976576, Elsevier: Scopus) Masashi Masuda, Shinobu Miyazaki-Anzai, Audrey L. Keenan, Yuji Shiozaki, Kayo Okamura, Wallace S. Chick, Kristina Williams, Xiaoyun Zhao, Shaikh Mizanoor Rahman, Yin Tintut, Christopher M. Adams and Makoto Miyazaki :
Activating transcription factor-4 promotes mineralization in vascular smooth muscle cells.,
JCI Insight, Vol.1, No.18, e88646, 2016.

(要約): Emerging evidence indicates that upregulation of the ER stress-induced pro-osteogenic transcription factor ATF4 plays an important role in vascular calcification, a common complication in patients with aging, diabetes, and chronic kidney disease (CKD). In this study, we demonstrated the pathophysiological role of ATF4 in vascular calcification using global Atf4 KO, smooth muscle cell-specific (SMC-specific) Atf4 KO, and transgenic (TG) mouse models. Reduced expression of ATF4 in global ATF4-haplodeficient and SMC-specific Atf4 KO mice reduced medial and atherosclerotic calcification under normal kidney and CKD conditions. In contrast, increased expression of ATF4 in SMC-specific Atf4 TG mice caused severe medial and atherosclerotic calcification. We further demonstrated that ATF4 transcriptionally upregulates the expression of type III sodium-dependent phosphate cotransporters (PiT1 and PiT2) by interacting with C/EBP . These results demonstrate that the ER stress effector ATF4 plays a critical role in the pathogenesis of vascular calcification through increased phosphate uptake in vascular SMCs.
(キーワード): Activating Transcription Factor 4 / Animals / Cells, Cultured / Humans / Ion Pumps / Male / Mice / Mice, Inbred C57BL / Mice, Inbred DBA / Mice, Knockout / Mice, Transgenic / Muscle, Smooth / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Vascular Calcification
(徳島大学機関リポジトリ): ● Metadata: 2007253
(出版サイトへのリンク): ● Publication site (DOI): 10.1172/jci.insight.88646
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27812542; ● Summary page in Scopus @ Elsevier: 2-s2.0-85055596087

(徳島大学機関リポジトリ: 2007253, DOI: 10.1172/jci.insight.88646, PubMed: 27812542, Elsevier: Scopus) 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.
(キーワード): Animals / Cell Cycle / Cells, Cultured / Familial Hypophosphatemic Rickets / Kidney / Male / Mice / Mice, Inbred C57BL / Mutation / Opossums / Phosphatidylinositol 4,5-Diphosphate / Sodium-Phosphate Cotransporter Proteins, Type IIc / Vacuoles
(徳島大学機関リポジトリ): ● Metadata: 2004468
(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: 2004468, DOI: 10.2152/jmi.62.209, PubMed: 26399350, Elsevier: Scopus) Hiroko Segawa, Yuji Shiozaki, Ichiro Kaneko and Ichi Ken Miyamoto :
The role of sodium-dependent phosphate transporter in phosphate homeostasis,
Journal of Nutritional Science and Vitaminology, Vol.61, S119-S121, 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.
(キーワード): Intestine / Kidney / Phosphate / Transporter
(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) 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: 2002357
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-84901390869

(徳島大学機関リポジトリ: 2002357, DOI: 10.1681/ASN.2013060569, PubMed: 24262791, Elsevier: Scopus) 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; ● Summary page in Scopus @ Elsevier: 2-s2.0-84860498827

(DOI: 10.1152/ajpcell.00314.2011, PubMed: 22159077, Elsevier: Scopus)

MISC

増田真志, 塩﨑雄治, 竹谷豊, 宮崎淳 :
最前線慢性腎臓病の合併症とlipotoxicity,
ファルマシア, Vol.58, No.4, 329-333, 2022年.

(徳島大学機関リポジトリ): ● Metadata: 2011398
(出版サイトへのリンク): ● Publication site (DOI): 10.14894/faruawpsj.58.4_329
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.14894/faruawpsj.58.4_329

(徳島大学機関リポジトリ: 2011398, DOI: 10.14894/faruawpsj.58.4_329) 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)

総説・解説

小宮蒼, 東彩生, 小池萌, 塩﨑雄治, 瀬川博子 :
リン代謝調節機構―腸管リン酸輸送の理解ー,
日本栄養・食糧学会誌, Vol.77, No.4, 247-253, 2024年4月. 小池萌, 東彩生, 小宮蒼, 塩﨑雄治, 瀬川博子 :
リン管理―CKD-MBDと栄養,
腎と透析, Vol.96, No.1, 112-116, 2024年1月.

(出版サイトへのリンク): ● Publication site (DOI): 10.24479/kd.0000001175
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390580793827920896; ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000001175

(DOI: 10.24479/kd.0000001175, CiNii: 1390580793827920896) 小池萌, 塩﨑雄治, 瀬川博子 :
無機リン酸の恒常性維持,
腎と透析, Vol.95, No.3, 267-271, 2023年9月.

(出版サイトへのリンク): ● Publication site (DOI): 10.24479/kd.0000000864
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390860620061733888; ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000864

(DOI: 10.24479/kd.0000000864, CiNii: 1390860620061733888) Megumi Koike, Minori Uga, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa :
Regulation of Phosphate Transporters and Novel Regulator of Phosphate Metabolism,
Endocrines, Vol.4, No.3, 607-615, Aug. 2023.

(出版サイトへのリンク): ● Publication site (DOI): 10.3390/endocrines4030043
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.3390/endocrines4030043

(DOI: 10.3390/endocrines4030043) 谷藤和也, 小池萌, 宇賀稔, 塩﨑雄治, 瀬川博子 :
Ca，Pホメオスタシス,
腎と透析, Vol.93, No.5, 736-741, 2022年11月.

(キーワード): 活性型ビタミンD / FGF23 / CaSR
(出版サイトへのリンク): ● Publication site (DOI): 10.24479/kd.0000000375
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390577133295330048; ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000375

(DOI: 10.24479/kd.0000000375, CiNii: 1390577133295330048) 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. 谷藤和也, 塩﨑雄治, 瀬川博子 :
骨を維持する栄養素,
体育の科学, Vol.71, No.11, 801-806, 2021年11月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520572360407947392

(CiNii: 1520572360407947392) Sawako Tatsumi, Atsumi Miyagawa, Ichiro Kaneko, Yuji Shiozaki, Hiroko Segawa and ichi Ken 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, Aug. 2015.

(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): Chronic kidney disease (CKD) / Inorganic phosphate / Inorganic phosphate transporters / Kidney-organ axis
(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; ● Summary page in Scopus @ Elsevier: 2-s2.0-84952875113

(DOI: 10.1007/s00774-015-0705-z, PubMed: 26296817, Elsevier: Scopus) Hiroko Segawa, 塩﨑雄治, Sakura Minoshima, ichi Ken Miyamoto :
[Updates on rickets and osteomalacia: the role of NaPi-2c/SLC34A3 and hypophosphataemic rickets].,
Clinical Calcium, Vol.23, No.10, 1445-1450, 2013年10月.

(要約): Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) , an autosomal recessive disorder first identified in a large Bedouin tribe, is characterized by hypophosphatemia secondary to renal inorganic phosphate (Pi) wasting, resulting in increased serum1,25-dihydroxyvitamin D3 concentrations with associated intestinal calcium hyperabsorption, hypercalciuria, rickets, and osteomalacia. Recent studies identified several mutations in the NaPi-2c/NPT2c transporter gene (SLC34A3) as the cause of HHRH. The fact that HHRH is caused by NaPi-2c loss-of-function mutations is compatible with the HHRH phenotype and the prevailing view of renal Pi regulation. The NaPi-2c mutants in HHRH show defective processing and stability.
(キーワード): Humans / Hypercalciuria / Kidney / Mutation / Rickets / Rickets, Hypophosphatemic / 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): 24076642; ● Summary page in Scopus @ Elsevier: 2-s2.0-84892735329

(PubMed: 24076642, Elsevier: Scopus) Shinsuke Kido, Kengo Nomura, Shohei Sasaki, 塩﨑雄治, Hiroko Segawa, Sawako Tatsumi :
[Information about phosphorus additives and nutritional counseling].,
Clinical Calcium, Vol.22, No.10, 1583-1591, 2012年10月.

(要約): Hyperphosphatemia is a common disorder in patients with chronic kidney disease (CKD) , and may result in hyperparathyroidism and renal osteodystrophy. Hyperphosphatemia also may contribute to deterioration vascular calcification and increase mortality. Hence, correction and prevention of hyperphosphatemia is a main component of the management of CKD. This goal is usually approached both by administering phosphorus binders and by restricting dietary phosphorus (P) intake. Dietary intake of phosphorus (P) is derived largely from foods with high protein content or food additives and is an important determinant of P balance in patient with CKD. Food additives (PO4) can dramatically increase the amount of P consumed in the daily diet, especially because P is more readily absorbed in its inorganic form. In addition, information about the P content and type in prepared foods is often unavailable or misleading. Therefore, during dietary counseling of patients with CKD, we recommended that they consider both the absolute dietary P content and the P-to-protein ratio of foods and meals including food additives.
(キーワード): Food Additives / Humans / Hyperphosphatemia / Phosphorus / Phosphorus, Dietary / Renal Dialysis / Renal Insufficiency, Chronic
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23023640; ● Summary page in Scopus @ Elsevier: 2-s2.0-84875110279

(PubMed: 23023640, Elsevier: Scopus) Shinsuke Kido, Marina Fujihara, Kengo Nomura, Shohei Sasaki, 塩﨑雄治, Hiroko Segawa, Sawako Tatsumi, ichi Ken Miyamoto :
[Fibroblast growth factor 23 mediates the phosphaturic actions of cadmium].,
日本衛生学雑誌, Vol.67, No.4, 464-471, 2012年.

(要約): Phosphaturia has been documented following cadmium (Cd) exposure in both humans and experimental animals. Fibroblast growth factor 23 (FGF23) serves as an essential phosphate homeostasis pathway in the bone-kidney axis. In the present study, we investigated the effects of Cd on phosphate (Pi) homeostasis in mice. Following Cd injection into C57BL/6J mice, plasma FGF23 concentration significantly increased. The urinary Pi excretion level was significantly higher in the Cd-injected C57BL/6J mice than in the control group. Plasma Pi concentration decreased only slightly in the Cd-injected mice compared with the control group. No changes were observed in the concentration of the plasma parathyroid hormone and 1,25-dihydroxy vitamin D(3) in both groups of mice. We observed a decrease in phosphate transport activity and also a decrease in the expression level of renal phosphate transporter Npt2c, but not that of Npt2a. Furthermore, we examined the effect of Cd on Npt2c in Npt2a-knockout (KO) mice, which expresses Npt2c as a major NaPi cotransporter. Injecting Cd to Npt2aKO mice induced a significant increase in plasma FGF23 concentration and urinary Pi excretion level. Furthermore, we observed decreases in phosphate transport activity and renal Npt2c expression level in the Cd-injected Npt2a KO mice. The present study suggests that hypophosphatemia induced by Cd may be closely associated with FGF23.
(キーワード): Animals / Biological Transport / Bone and Bones / Cadmium / Fibroblast Growth Factor-23 / Fibroblast Growth Factors / Homeostasis / Humans / Hypophosphatemia / Hypophosphatemia, Familial / Kidney / Mice / Mice, Inbred C57BL / Osteomalacia / Phosphates / Sodium-Phosphate Cotransporter Proteins, Type IIa / Sodium-Phosphate Cotransporter Proteins, Type IIc
(出版サイトへのリンク): ● Publication site (DOI): 10.1265/jjh.67.464
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23095356; ● Summary page in Scopus @ Elsevier: 2-s2.0-84879323850

(DOI: 10.1265/jjh.67.464, PubMed: 23095356, Elsevier: Scopus)

講演・発表

Yuji Shiozaki, UGA Minori, Megumi Koike, KOMIYA Aoi, SHIBAHARA Shion, Ayami Higashi, Ken-ichi Miyamoto and Hiroko Segawa :
Identification of functional domains of TMEM174 on PTH-induced endocytosis of NaPi2a,
Physiology, Biology and Pathology of Phosphate Gordon Research Conference, Renaissance Tuscany Il Ciocco, Via Giovanni Pascoli, Lucca, Italy, Feb. 2025. 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. Minori Uga, Ichiro Kaneko, Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Yuji Shiozaki, Peter W. Jurutka and Hiroko Segawa :
The role of intestinal Cytochrome P450 in vitamin D metabolism,
22nd International Congress of Nutrition in Tokyo, Dec. 2022. 柴原しおん, 塩﨑雄治, 宇賀穂, 小宮蒼, 東彩生, 大森みのり, 谷井颯花, 小池萌, 瀬川博子 :
IP6K-Xpr1阻害剤の近位尿細管細胞NaPi2a発現及びリン酸輸送活性に対する作用の解明,
第 57 回日本栄養・食糧学会中国・四国支部大会, 2024年11月. 東彩生, 小宮蒼, 石川茜, 柴原しおん, 宇賀穂, 小池萌, 塩﨑雄治, 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と解析,
第12回日本腎栄養代謝研究会学術集会・総会, 2024年8月. 小宮蒼, 小池萌, 宇賀穂, 東彩生, 石川茜, 柴原しおん, 塩﨑雄治, 宮本賢一, 瀬川博子 :
NEP25 Tgマウス CKD-MBDモデルを用いた新規リン代謝調節機構の解明,
第9回日本栄養改善学会四国支部学術総会, 2024年6月. 小池萌, 東彩生, 小宮蒼, 塩﨑雄治, 宇賀穂, 柴原しおん, 宮本賢一, 瀬川博子 :
成長を制御する新規システム-ミネラル代謝・抗老化因子 α-klotho-,
第78回日本栄養・食糧学会大会, 2024年5月. 塩﨑雄治, 濱口ゆき, 宇賀穂, 柴原しおん, 小宮蒼, 東彩生, 石川茜, 小池萌, 宮本賢一, 瀬川博子 :
腎臓リン酸再吸収機構におけるリン酸排出トランスポーターXpr1の役割,
第78回日本栄養・食糧学会大会, 2024年5月. 塩﨑雄治, 濵口ゆき, 宇賀穂, 柴原しおん, 小宮蒼, 東彩生, 石川茜, 小池萌, 宮本賢一, 瀬川博子 :
腎臓リン酸再吸収機構におけるリン酸排出トランスポーターXpr1の役割,
第78回日本栄養・食糧学会大会, 2024年4月. 塩﨑雄治 :
Tmem174によるNaPi2a制御についての最新知見,
第8回CKD-MBD学会学術集会・総会, 2024年3月. 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. 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. 宇賀穂, 金子一郎, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 小宮蒼, 原田和, 浜口ゆき, 三浦美月, 塩﨑雄治, 瀬川博子 :
小腸Cytochrome P450(CYP3A)がビタミンD活性に及ぼす影響,
第54回日本栄養・食糧学会中国・四国支部大会・第7回日本栄養改善学会四国支部学術総会合同大会, 2021年10月. 川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, 塩﨑雄治, 金子一郎, 瀬川博子 :
ライフステージに着目した生体内リン代謝の性差検討,
第68回日本栄養改善学会学術総会, 2021年10月. 川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, 塩﨑雄治, 金子一郎, 瀬川博子 :
ライフステージに着目した生体内リン代謝の性差検討,
第75回日本栄養・食糧学会大会, 2021年7月.

研究会・報告書: 原田和, 宇賀穂, 小宮蒼, 東彩生, 三浦美月, 柴原しおん, 小池萌, 塩﨑雄治, 瀬川博子 :
新規リン代謝調節因子Tmem174の血中リン濃度調節における役割,
第7回日本Uremic Toxin研究会学術集会, 2024年4月. 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, 瀬川博子 :
腎リン酸トランスポーターの機能制御と疾患,
第16回トランスポーター研究会年会, 2022年7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.

特許: 研究者総覧に該当データはありませんでした。
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補助金・競争的資金: リン酸排出トランスポーター制御による寝たきり予防：破骨細胞とリン動態の解析 (研究課題/領域番号: 24K14626 )
細胞内リン酸排出分子XPR1による抗組織老化作用の解明 (研究課題/領域番号: 22K17800 )
小腸FGF19産生・分泌を基盤とした健康長寿を目指す栄養療法 (研究課題/領域番号: 21K11594 )
抗老化因子を制御するミネラル栄養学の確立 (研究課題/領域番号: 21H03375 )
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所属学会・所属協会: 日本栄養·食糧学会
米国腎臓学会
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受賞: 2023年3月, 優秀演題賞受賞 (日本CKD-MBD学会)
2023年5月, 優秀演題賞受賞 (第6回日本Uremic Toxin研究会学術集会)
2024年3月, 医学部ベストティーチャー・オブ・ザ・イヤー2023 (徳島大学)
2024年3月, 令和5年度岡奨学賞 (徳島大学)
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氏名（漢字）: 塩﨑雄治
氏名（フリガナ）: シオザキユウヂ
氏名（英字）: Shiozaki Yuji
所属機関: 徳島大学大学院助教

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researchmap最終確認日: 2025/5/4 03:40
氏名（漢字）: 塩﨑雄治
氏名（フリガナ）: シオザキユウヂ
氏名（英字）: Shiozaki Yuji
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