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阪上浩

徳島大学

プロフィール
教育活動
研究活動
社会活動
リサーチマップ・
Jグローバル
KAKEN
注目研究

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2020年12月4日更新

職名: 教授
性別: 男
生年: 1960
電話: 088-633-7091
電子メール: hsakaue@nutr.med.tokushima-u.ac.jp
学歴: 1989/3: 神戸大学医学部医学科卒業
学位: 博士(医学) (神戸大学) (1998年3月)
職歴・経歴: 2009/2: 徳島大学准教授, 大学院ヘルスバイオサイエンス研究部 (-2014.9.)
2014/10: 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

専門分野・研究分野: 糖尿病・肥満

研究者総覧で最新データを確認する

2020年12月4日更新

専門分野・研究分野: 糖尿病・肥満
担当経験のある授業科目: SIH道場~アクティブ・ラーニング入門~(医・医科栄養) (共通教育)
がんチーム医療実習 (大学院)
がん治療と栄養管理 (大学院)
ライフステージ栄養学総合演習 (学部)
健康医科学セミナー (大学院)
健康医科学実験 (大学院)
健康医科学演習 (大学院)
健康医科学特別実験 (大学院)
公衆衛生学 (学部)
医療倫理と法律的・経済的問題 (大学院)
医療対話学(コミュニケーションスキル) (大学院)
医療情報学 (大学院)
医療栄養学概論 (大学院)
医療栄養学特論 (大学院)
宇宙と栄養・医学概論 (大学院)
心身健康と環境ストレス (大学院)
応用栄養学実習 (学部)
応用栄養学演習 (学部)
悪性腫瘍の管理と治療 (大学院)
栄養と薬 (学部)
栄養サポート概論 (大学院)
栄養教育論2 (学部)
栄養教育論実習 (学部)
栄養英語 (学部)
生命科学の研究手法 (大学院)
疾患栄養管理学Ⅱ (学部)
研究方法論 (大学院)
緩和ケアと栄養 (大学院)
腫瘍栄養学各論 (大学院)
臨床代謝栄養学Ⅰ (大学院)
臨床代謝栄養学Ⅱ (大学院)
臨床医学入門 (学部)
臨床栄養学概論 (大学院)
臨床栄養管理学Ⅰ (大学院)
指導経験: 1人 (学士), 3人 (修士)

研究者総覧で最新データを確認する

2020年12月4日更新

専門分野・研究分野: 糖尿病・肥満

研究テーマ: 脂肪細胞の分化・増殖機構とライフサイクルの解明に関する研究, 脂肪細胞制御によるメタボリックシンドローム治療法の開発に関する研究 (糖尿病 (diabetes), 肥満症 (obesity), 脂肪細胞 (adipocyte), アディポサイトカイン (adipocytekine), 細胞増殖·分化 (cell proliferation and differentiation), 転写因子 (transcription factor))

著書

武田英二, 鈴木佳子, 松村晃子, 中屋豊, 堤理恵, 阪上浩, 濵田康弘, 秦明子, 他42人 :
認定NSTガイドブック2017 改訂第5版,
2017年7月. 竹谷豊, 塚原丘美, 桑波田雅士, 阪上浩 :
新・臨床栄養学 (栄養科学シリーズNEXT) 改訂,
株式会社講談社, 2016年1月. 堤理恵, 阪上浩, 堤保夫 :

2015年8月. 新井英一, 阪上浩, 武田英二, 竹谷豊, 藤岡由夫, 細川雅也 :
臨床病態栄養学第3版,
文光堂, 2013年9月. 岡田裕子, 阪上浩, 春日雅人 :
肥満症のくすり,
日本評論社, 2011年4月. 阪上浩 :
がん栄養ハンドブック,
メディカルレビュー社, 大阪, 2011年1月. 阪上浩 :
NSTガイドブック2011 リフィーディング症候群の予防と治療,
メディカルレビュー社, 2011年1月. 阪上浩 :
糖尿病ナビゲーター脂肪細胞分化,
メディカルレビュー社, 2010年9月.

論文

Yumiko Miyatake, Yuna Mishima, Rie Tsutsumi, Tamaki Otani, Naoya Suemasa, Saeko Masumoto, Masashi Kuroda and Hiroshi Sakaue :
Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging.,
Biochemical and Biophysical Research Communications, Vol.528, No.3, 499-505, 2020.

(要約): Measuring glucose uptake in the skeletal muscle in vivo is an effective method to determine glucose metabolism abnormalities as the skeletal muscle is the principal tissue responsible for glucose disposal and is a major site of peripheral insulin resistance. In this study, we investigated the pathological glucose metabolism dynamics of the skeletal muscle of C57BL/6J mice in a noninvasive and time-sequential manner using positron emission tomography/computed tomography (PET/CT), an imaging technique that uses radioactive substances to visualize and measure metabolic processes in the body, with [
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2020.05.165
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32513534; ● Search Scopus @ Elsevier (PMID): 32513534; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.05.165

(DOI: 10.1016/j.bbrc.2020.05.165, PubMed: 32513534) Nagakatsu Harada, Yuka Gotoda, Adzumi Hatakeyama, Tadahiko Nakagawa, Yumiko Miyatake, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue :
Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes.,
Journal of Muscle Research and Cell Motility, 2020.

(要約): ACTN2 and ACTN3 encode sarcomeric α-actinin-2 and α-actinin-3 proteins, respectively, that constitute the Z-line in mammalian skeletal muscle fibers. In human ACTN3, a nonsense mutation at codon 577 that encodes arginine (R) produces the R577X polymorphism. Individuals having a homozygous 577XX genotype do not produce α-actinin-3 protein. The 577XX genotype reportedly occurs in sprint and power athletes in frequency lower than in the normal population, suggesting that α-actinin-3 deficiency diminishes fast-type muscle function. Among humans who carry 577R alleles, varying ACTN3 expression levels under certain conditions can have diverse effects on atheletic and muscle performance. However, the factors that regulate ACTN3 expression are unclear. Here we investigated whether the unfolded protein response (UPR) under endoplasmic reticulum (ER) stress regulates expression of Actn3 and its isoform Actn2 in mouse C2C12 myotubes. Among UPR-related transcription factors, XBP1 upregulated Actn2, whereas XBP1, ATF4 and ATF6 downregulated Actn3 promoter activity. Chemical induction of ER stress increased Actn2 mRNA levels, but decreased those for Actn3. ER stress also decreased α-actinin-3 protein levels, whereas levels of α-actinin-2 were unchanged. The intracellular composition of muscle contraction-related proteins was altered under ER stress, in that expression of parvalbumin (a fast-twitch muscle-specific protein) and troponin I type 1 (skeletal, slow) was suppressed. siRNA-induced suppression of Actn3 mimicked the inhibitory effect of ER stress on parvalbumin levels. Thus, endogenous expression levels of α-actinin-3 can be altered by ER stress, which may modulate muscle performance and athletic aptitudes, particularly in humans who carry ACTN3 577R alleles.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10974-020-09582-7
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32451822; ● Search Scopus @ Elsevier (PMID): 32451822; ● Search Scopus @ Elsevier (DOI): 10.1007/s10974-020-09582-7

(DOI: 10.1007/s10974-020-09582-7, PubMed: 32451822) Masashi Kuroda, Misa Nishiguchi, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Yumiko Miyatake, Mayu Sebe, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue :
Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription.,
PLoS ONE, Vol.15, No.5, e0233390, 2020.

(要約): Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity.
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0233390
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32437400; ● Search Scopus @ Elsevier (PMID): 32437400; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0233390

(DOI: 10.1371/journal.pone.0233390, PubMed: 32437400) Tetsuya Hosooka, Yusei Hosokawa, Kaku Matsugi, Masakazu Shinohara, Yoko Senga, Yoshikazu Tamori, Chikako Aoki, Sho Matsui, Tsutomu Sasaki, Tadahiro Kitamura, Masashi Kuroda, Hiroshi Sakaue, Kazuhiro Nomura, Kei Yoshino, Yuko Nabatame, Yoshito Itoh, Kanji Yamaguchi, Yoshitake Hayashi, Jun Nakae, Domenico Accili, Takehiko Yokomizo, Susumu Seino, Masato Kasuga and Wataru Ogawa :
The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B 4 axis,
Proceedings of the National Academy of Sciences of the United States of America, Vol.117, No.21, 11674-11684, 2020.

(要約): Although adipocytes are major targets of insulin, the influence of impaired insulin action in adipocytes on metabolic homeostasis remains unclear. We here show that adipocyte-specific PDK1 (3'-phosphoinositide-dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipose tissue mass. A-PDK1KO mice developed insulin resistance, glucose intolerance, and hepatic steatosis, and this phenotype was suppressed by additional ablation of FoxO1 specifically in adipocytes (A-PDK1/FoxO1KO mice) without an effect on adipose tissue mass. Neither circulating levels of adiponectin and leptin nor inflammatory markers in adipose tissue differed between A-PDK1KO and A-PDK1/FoxO1KO mice. Lipidomics and microarray analyses revealed that leukotriene B4 (LTB4) levels in plasma and in adipose tissue as well as the expression of 5-lipoxygenase (5-LO) in adipose tissue were increased and restored in A-PDK1KO mice and A-PDK1/FoxO1KO mice, respectively. Genetic deletion of the LTB4 receptor BLT1 as well as pharmacological intervention to 5-LO or BLT1 ameliorated insulin resistance in A-PDK1KO mice. Furthermore, insulin was found to inhibit LTB4 production through down-regulation of 5-LO expression via the PDK1-FoxO1 pathway in isolated adipocytes. Our results indicate that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK1-FoxO1 pathway and thereby maintains systemic insulin sensitivity.
(出版サイトへのリンク): ● Publication site (DOI): 10.1073/pnas.1921015117
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32393635; ● Search Scopus @ Elsevier (PMID): 32393635; ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.1921015117

(DOI: 10.1073/pnas.1921015117, PubMed: 32393635) Masashi Masuda, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiroh Adachi, Kohta Ohnishi, Hirokazu Ohminami, Hisami Yamanaka-Okumura, Hiroshi Sakaue, Makoto Miyazaki, Eiji Takeda and Yutaka Taketani :
All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b).,
The Biochemical Journal, Vol.477, No.4, 817-831, 2020.

(要約): Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Although we previously reported that vitamin A-deficient (VAD) rats had increased urine Pi excretion through the decreased renal expression of Npt2a and Npt2c, the effect of vitamin A on the intestinal Npt2b expression remains unclear. In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. The transcriptional activity of reporter plasmid containing the promoter region of the rat Npt2b gene was reduced by ATRA in NIH3T3 cells overexpressing retinoic acid receptor (RAR) and retinoid X receptor (RXR). On the other hand, CCAAT/enhancer-binding proteins (C/EBP) induced transcriptional activity of the Npt2b gene. Knockdown of the C/EBP gene and a mutation analysis of the C/EBP responsible element in the Npt2b gene promoter indicated that C/EBP plays a pivotal role in the regulation of Npt2b gene transcriptional activity by ATRA. EMSA revealed that the RAR/RXR complex inhibits binding of C/EBP to Npt2b gene promoter. Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene.
(徳島大学機関リポジトリ): ● Metadata: 114417
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/BCJ20190716
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32016357; ● Search Scopus @ Elsevier (PMID): 32016357; ● Search Scopus @ Elsevier (DOI): 10.1042/BCJ20190716

(徳島大学機関リポジトリ: 114417, DOI: 10.1042/BCJ20190716, PubMed: 32016357) Masashi Kuroda, Rumi Onoyama, Waka Sasaki, Mayu Sebe, Tadahiro Kitamura, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue :
DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression.,
Biochemical and Biophysical Research Communications, Vol.525, No.1, 39-45, 2020.

(要約): Researchers frequently use 3T3-L1 adipocytes as a fat cell line, but the capacity of this line for insulin-mediated glucose transport is lower than that of primary isolated fat cells. In this study, we found that 5-azacytidine (5-aza-C), DNA methyltransferase 1 inhibitor, enhanced insulin-stimulated 2-deoxyglucose (2-DG) transport in 3T3-L1 cells after adipogenic differentiation. We next examined the expression of the genes related to glucose transport and insulin signal transduction. The insulin independent glucose transporter, glucose transporter 1 (GLUT1), showed lower expression in 5-aza-C pre-treated 3T3-L1 adipocytes, than in un-treated control adipocytes, while the expression of insulin dependent transporter GLUT4 remained unchanged. In addition, insulin receptor substrate-1 (IRS-1) was highly expressed in 5-aza-C pre-treated adipocytes. Based on DNA microarray and functional annotation analysis, we noticed that 5-aza-C pretreatment activated the tumor suppressor p53 pathway. We confirmed that in 5-aza-C adipocytes, p53 expression was markedly higher, and the methylation level of CpGs in its promoter region was lower than in un-treated control adipocytes. Moreover, pharmacological inhibition of p53 restored GLUT1 and IRS-1 expression to the same level as in un-treated 3T3-L1 adipocytes, and significantly decreased insulin-mediated 2-DG uptake. These results suggest that glucose transport capacity in adipocytes is influenced by DNA methylation status, and demethylation induced by 5-aza-C increased it possibly through the p53 signaling pathway.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2020.02.038
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32070490; ● Search Scopus @ Elsevier (PMID): 32070490; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2020.02.038

(DOI: 10.1016/j.bbrc.2020.02.038, PubMed: 32070490) Taigo Horiguchi, Yumiko Miyake, Keiko Miyoshi, Ayako Tanimura, Hiroko Hagita, Hiroshi Sakaue and Takafumi Noma :
Gene-expression profile reveals the genetic and acquired phenotypes of hyperactive mutant SPORTS rad,
The Journal of Medical Investigation : JMI, Vol.VOL67, No.NO1,2, 51-61, 2020.

(要約): Spontaneously Running Tokushima Shikoku (SPORTS) rat is a hyperactive rat strain. However, the causative mutation of this phenotype has not yet been identified. To investigate the molecular basis for the unique phenotype of SPORTS rats, we examined gene-expression profiles by microarray analyses. Among adenylate kinase isozymes that maintain the homeostasis of cellular adenine nucleotide composition in the cell, only adenylate kinase 1 is highly up-regulated in both exercised and sedentary SPORTS rats compared with wild-type (WT) rats, 5.5-fold and 3.3-fold, respectively. Further comparative analyses revealed that genes involved in glucose metabolism were up-regulated in skeletal muscle tissue of exercised SPORTS rats compared with sedentary mutants, whereas genes related to extracellular matrix or region were down-regulated compared with WT rats. In brain tissue of sedentary SPORTS rats, genes associated with defense and catecholamine metabolism were highly expressed compared with WT rats. These findings suggest that genetic mutation(s) in SPORTS rat remodels metabolic demands through differentially regulating gene expression regardless of exercise. Therefore, the SPORTS rats are useful animal model not only for further examining the effects of exercise on metabolism but also for deeply studying the molecular basis how mutation affect the psychological motivation with spontaneous voluntary exercise phenotype. J. Med. Invest. 67 : 51-61, February, 2020.
(徳島大学機関リポジトリ): ● Metadata: 114556
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.67.51
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378618; ● Search Scopus @ Elsevier (PMID): 32378618; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.51

(徳島大学機関リポジトリ: 114556, DOI: 10.2152/jmi.67.51, PubMed: 32378618) Nobuto Nakanishi, Rie Tsutsumi, Yoshihiro Okayama, Takuya Takashima, Yoshitoyo Ueno, Taiga Itagaki, Yasuo Tsutsumi, Hiroshi Sakaue and Jun Oto :
Monitoring of muscle mass in criticaly ill patients: comparison of ultrasound and two bioelectrical impedance analysis devices,
Journal of Intensive Care, Vol.7, 61, 2020.

(要約): Skeletal muscle atrophy commonly occurs in critically ill patients, and decreased muscle mass is associated with worse clinical outcomes. Muscle mass can be assessed using various tools, including ultrasound and bioelectrical impedance analysis (BIA). However, the effectiveness of muscle mass monitoring is unclear in critically ill patients. This study was conducted to compare ultrasound and BIA for the monitoring of muscle mass in critically ill patients. We recruited adult patients who were expected to undergo mechanical ventilation for > 48 h and to remain in the intensive care unit (ICU) for > 5 days. On days 1, 3, 5, 7, and 10, muscle mass was evaluated using an ultrasound and two BIA devices (Bioscan: Malton International, England; Physion: Nippon Shooter, Japan). The influence of fluid balance was also evaluated between each measurement day. We analyzed 93 images in 21 patients. The age of the patients was 69 (interquartile range, IQR, 59-74) years, with 16 men and 5 women. The length of ICU stay was 11 days (IQR, 9-25 days). The muscle mass, monitored by ultrasound, decreased progressively by 9.2% (95% confidence interval (CI), 5.9-12.5%), 12.7% (95% CI, 9.3-16.1%), 18.2% (95% CI, 14.7-21.6%), and 21.8% (95% CI, 17.9-25.7%) on days 3, 5, 7, and 10 ( < 0.01), respectively, with no influence of fluid balance ( = 0.04, = 0.74). The muscle mass did not decrease significantly in both the BIA devices (Bioscan, = 0.14; Physion, = 0.60), and an influence of fluid balance was observed (Bioscan, = 0.37, < 0.01; Physion, = 0.51, < 0.01). The muscle mass assessment at one point between ultrasound and BIA was moderately correlated (Bioscan, = 0.51, < 0.01; Physion, = 0.37, < 0.01), but the change of muscle mass in the same patient did not correlate between these two devices (Bioscan, = - 0.05, = 0.69; Physion, = 0.23, = 0.07). Ultrasound is suitable for sequential monitoring of muscle atrophy in critically ill patients. Monitoring by BIA should be carefully interpreted owing to the influence of fluid change. UMIN000031316. Retrospectively registered on 15 February 2018.
(キーワード): 超音波 (ultrasound) / Bioelectrical impedance analysis / 筋萎縮 (muscle atrophy)
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s40560-019-0416-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31890223; ● Summary page in Scopus @ Elsevier: 2-s2.0-85077117012

(DOI: 10.1186/s40560-019-0416-y, PubMed: 31890223, Elsevier: Scopus) Shiho Satomi, Atsushi Morio, Hirotsugu Miyoshi, Ryuji Nakamura, Rie Tsutsumi, Hiroshi Sakaue, Toshimichi Yasuda, Noboru Saeki and Yasuo M. Tsutsumi :
Branched-chain amino acids-induced cardiac protection against ischemia/reperfusion injury.,
Life Sciences, Vol.245, 2020.

(要約): Mice treated with BCAAs had a significant reduction in infarct size as a percentage of the area at risk compared to controls (34.1 ± 3.9% vs. 44.7 ± 2.6%, P = 0.001), whereas mice treated with the mTOR inhibitor rapamycin were not protected by BCAA administration (42.2 ± 6.5%, vs. control, P = 0.015). This protection was not detected in our hetero knockout mice of mTOR. Western blot analysis revealed no change in AKT signaling whereas activation of mTOR was identified. Furthermore, BCAAs prevented swelling which was reversed by the addition of rapamycin. In myocytes undergoing simulated I/R, BCAA treatment significantly preserved cell viability (71.7 ± 2.7% vs. 34.5 ± 1.6%, respectively, p < 0.0001), whereas rapamycin prevented this BCAA-induced cardioprotective effect (43.5 ± 3.4% vs. BCAA, p < 0.0001).
(キーワード): Amino Acids, Branched-Chain / Animals / Blotting, Western / Cardiotonic Agents / Disease Models, Animal / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Myocardial Reperfusion Injury / Myocytes, Cardiac / Rats / Rats, Wistar / Sirolimus / TOR Serine-Threonine Kinases
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.lfs.2020.117368
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32001270; ● Summary page in Scopus @ Elsevier: 2-s2.0-85078659582

(DOI: 10.1016/j.lfs.2020.117368, PubMed: 32001270, Elsevier: Scopus) Mayu Sebe, Rie Tsutsumi, Takuro Oyama, T Yousuke Horikawa, Yuta Uemura, Nami Kakuta, Yoko Sakai, Atsushi Morio, Hirotsugu Miyoshi, Takashi Kondo, Tomoaki Urabe, Yuko Noda, Satoshi Kamiya, Noboru Saeki, Masashi Kuroda, Katsuya Tanaka, Yasuo Tsutsumi and Hiroshi Sakaue :
Assessment of postoperative nutritional status and physical function between open surgical aortic valve replacement and transcatheter aortic valve implantation in elderly patients.,
The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 139-144, 2020.

(要約): Background and aims : Severe aortic stenosis (AS) has been normally treated with surgical aortic valve replacement (AVR) whereas recently, transcatheter aortic valve implantation (TAVI) has been introduced as a minimally invasive operation for patients with high surgical risk and frailty. In this study, we have evaluated postoperative physical function and nutrition intake in the patients following AVR and TAVI. Methods : This prospective observational study involved 9 patients with surgical aortic valve replacement (AVR) and 7 patients with transcatheter aortic valve implantation (TAVI). Body composition was measured one day prior surgery, postoperative day (POD) 1, POD 3, POD 5 and POD 7. Hand grip strength, calf circumference and gait speed were measured one day before surgery and on the day of discharge. Results : Skeletal muscle was significantly decreased in AVR patients at postoperative day 3 and 7, while there was no change in TAVI patients. Patients with TAVI showed higher dietary intake after surgery compared to patients with AVR, and they maintained hand grip strength and calf circumference at discharge. Conclusions : In elderly patients with AS, TAVI can improve post-operative recovery maintaining nutritional status and physical function even. J. Med. Invest. 67 : 139-144, February, 2020.
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.67.139
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378597; ● Search Scopus @ Elsevier (PMID): 32378597; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.139

(DOI: 10.2152/jmi.67.139, PubMed: 32378597) Tetsuya Shiuchi, Yumiko Miyatake, Airi Otsuka, Sachiko Chikahisa, Hiroshi Sakaue and Hiroyoshi Sei :
Role of orexin in exercise-induced leptin sensitivity in the mediobasal hypothalamus of mice.,
Biochemical and Biophysical Research Communications, Vol.514, No.1, 166-172, 2019.

(要約): Orexin is known as an important neuropeptide in the regulation of energy metabolism. However, the role of orexin in exercise-induced leptin sensitivity in the hypothalamus has been unclear. In this study, we determined the effect of transient treadmill exercise on leptin sensitivity in the mediobasal hypothalamus (MBH) of mice and examined the role of orexin in post-exercise leptin sensitivity. Treadmill running for 45min increased the orexin neuron activity in mice. Intraperitoneal injection of a submaximal dose of leptin after exercise stimulated the phosphorylation of signal transducer and activator of transcription 3 (STAT3) in MBH of mice post-exercise compared with that in non-exercised mice, although intracerebroventricular (icv) injection of leptin did not enhance STAT3 phosphorylation, even after exercise. Icv injection of an orexin receptor antagonist, SB334867 reduced STAT3 phosphorylation, which was enhanced by icv injection of orexin but not by direct injection of orexin into MBH. Exercise increased the phosphorylation of extracellular signal-regulated kinases (ERKs) in the MBH of mice, while ERK phosphorylation was reduced by SB334867. Leptin injection after exercise increased the leptin level in MBH, whereas icv injection of SB334867 suppressed the increase in the leptin level in MBH of mice. These results indicate that the activation of orexin neurons by exercise may contribute to the enhancement of leptin sensitivity in MBH. This effect may be mediated by increased transportation of circulating leptin into MBH, with the involvement of ERK phosphorylation.
(徳島大学機関リポジトリ): ● Metadata: 115013
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2019.04.145
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31029425; ● Search Scopus @ Elsevier (PMID): 31029425; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2019.04.145

(徳島大学機関リポジトリ: 115013, DOI: 10.1016/j.bbrc.2019.04.145, PubMed: 31029425) Masahiro Bando, Saeko Masumoto, Masashi Kuroda, Rie Tsutsumi and Hiroshi Sakaue :
Effect of olive oil consumption on aging in a senescence-accelerated mice-prone 8 (SAMP8) model.,
The Journal of Medical Investigation : JMI, Vol.66, No.3.4, 241-247, 2019.

(要約): Background : Mediterranean diets have been linked to a reduced risk of cancer, vascular illnesses, Parkinson's and Alzheimer's disease. Olive oil is the primary fat source in the Mediterranean diet ; however, only a few studies have investigated the effect of olive oil on aging. In the present study, we aimed to determine whether consumption of olive oil significantly influences aging and memory in senescence-accelerated mouse-prone 8 (SAMP8). Methods : SAMP8 and senescence-accelerated mouse resistant 1 (SAMR1) mice were fed either 7% soy oil or 1% olive oil and 6% soy oil during a six-month study period. Reduction in memory in passive avoidance learning was examined after two months from the initiation of the experiment. Results : The weight of organs including the liver, kidney, spleen, and fat tissue changed significantly and memory performance was reduced in SAMP8 than in SAMR1 mice. There were no significant differences in SAMP8 and SAMR1 mice; however, blood triglyceride level decreased significantly in SAMP8 mice fed on olive oil. Conclusions : These results suggest that consuming olive oil may not have a protective role in aging and memory recall, but beneficial effects may be related to improvement in lipid metabolism. J. Med. Invest. 66 : 241-247, August, 2019.
(キーワード): Aging / Animals / Avoidance Learning / Diet, Mediterranean / 記憶 (memory) / Mice / Models, Animal / Olive Oil / Organ Size / Triglycerides
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.66.241
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31656282; ● Search Scopus @ Elsevier (PMID): 31656282; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.241

(DOI: 10.2152/jmi.66.241, PubMed: 31656282) 堤理恵, 瀬部真由, 別府香名, 渡辺涼乃, 尾平優, 黒田雅士, 阪上浩 :
化学療法に伴う味覚・嗅覚障害への対応 (特集化学療法時の栄養管理),
日本静脈経腸栄養学会雑誌, Vol.33, No.4, 1019-1024, 2018年.

(徳島大学機関リポジトリ): ● Metadata: 113717
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (NAID): 40021698908

(徳島大学機関リポジトリ: 113717, CiNii: 40021698908) 松島里那, 堤理恵, 庄野仁志, 別府香名, 渡辺涼乃, 尾平優, 黒田雅士, 武田憲昭, 阪上浩 :
第38回徳島医学会賞受賞論文がん治療中の味覚変化と食事介入の取り組み,
四国医学雑誌, Vol.74, No.3, 101-106, 2018年.

(要約): For patients with cancer, malnutrition is one of the most serious problems. Cancer treatments, such as chemotherapy and radiotherapy, are effective for metastasis and tumor reduction as adjuvant therapy at the perioperative stage, in addition to prolonging the life of a patient and providing a radical cure. On the other hand, loss of appetite that is induced by the above treatment sometimes worsens the nutritional health of a patient. Therefore, it confers prolonged hospitalization and a delay in additional chemotherapy or surgery. Moreover, other side effects besides the loss of appetite due to chemoradiotherapy(hair loss, nausea, vomiting, and diarrhea, among others)can lead to worse nutritional health. Among these side effects, taste disorder is a major factor of decreasing meal intake and is a severe problem occurring frequently during treatment. However, its fundamental reasons, remedial measures, and treatments have not been established yet. In this article, we will report the previous basic research and clinical problems of dysgeusia that occurs during cancer treatment, and introduce a nutritional approach to preventing or improving dysgeusia.
(徳島大学機関リポジトリ): ● Metadata: 112298
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (NAID): 120006531553

(徳島大学機関リポジトリ: 112298, CiNii: 120006531553) Nagakatsu Harada, Adzumi Hatakeyama, Maiko Okuyama, Yumiko Miyatake, Tadahiko Nakagawa, Masashi Kuroda, Saeko Masumoto, Rie Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue :
Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein.,
Biochemical and Biophysical Research Communications, Vol.502, No.3, 422-428, 2018.

(要約): , respectively) and transfected the constructs into HEK293 cells. Similar constructs for the ACTN3 577R gene were used as controls. HEK293 cells carrying the X gene, but not the X
(キーワード): Actinin / Caffeine / Codon, Nonsense / Gentamicins / HEK293 Cells / Humans / Muscle, Skeletal / Mutant Proteins / Peptide Chain Termination, Translational / RNA Stability / RNA, Messenger / Transfection
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2018.05.193
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29857001; ● Search Scopus @ Elsevier (PMID): 29857001; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.05.193

(DOI: 10.1016/j.bbrc.2018.05.193, PubMed: 29857001) Manami Abe, Yuki Matsuo, Akiko Harada, Takayuki Uchida, Kanako Kitahata, Chisato Tomida, Katsuya Hirasaka, Shigetada Kondo, Nagakatsu Harada, Yutaka Nakaya, Hiroshi Sakaue, Reiko Nakao and Takeshi Nikawa :
Distinct Gene Expression Profile Distinguishes Increased Metabolic Activity in Spontaneously Hyperactive Rats While Sedentary from That Induced by Exercise,
Advances in Biological Chemistry, Vol.8, No.01, 1-14, 2018.

(徳島大学機関リポジトリ): ● Metadata: 111609
(出版サイトへのリンク): ● Publication site (DOI): 10.4236/abc.2018.81001
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.4236/abc.2018.81001

(徳島大学機関リポジトリ: 111609, DOI: 10.4236/abc.2018.81001) Chikugo Momoko, Sebe Mayu, Rie Tsutsumi, Iuchi Marina, Jun Kishi, Masashi Kuroda, Nagakatsu Harada, Yasuhiko Nishioka and Hiroshi Sakaue :
Effect of Janus kinase inhibition by tofacitinib on body composition and glucose metabolism.,
The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 166-170, 2018.

(要約): Tofacitinib is the first Janus Kinase (JAK) inhibitor to treat moderately to severely active RA. In this study, we investigated whether the effect of tofacitinib have any effects on body composition in mice and female patients with RA. Female C57BL/6 mice fed with a high-fat diet were treated with 30 mg/kg/day tofacitinib or vehicle for 70 days. Following treatment, trunk muscle, subcutaneous fat, and visceral fats were measured using X-ray computed tomography CT scan. Glucose tolerance and insulin sensitivity were assessed. In female RA patients treated with biological disease modified anti-rheumatic-drugs (biological DMARDs) or tofacitinib (n=4 per group), we also evaluated the body composition after 3 months from the start of treatment initiation using bioelectrical impedance analysis. Treatment with tofacitinib did not affect the body weight, and body composition in C57BL/6 mice. It also did not affect glucose, and insulin tolerance in mice. In patients with RA, treatment with biological DMARDs did not affect the body composition whereas the muscle mass was unchanged after receiving tofacitinib and the fat mass was significantly increased. J. Med. Invest. 65:166-170, August, 2018.
(徳島大学機関リポジトリ): ● Metadata: 112232
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.65.166
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282855; ● Search Scopus @ Elsevier (PMID): 30282855; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.166

(徳島大学機関リポジトリ: 112232, DOI: 10.2152/jmi.65.166, PubMed: 30282855) Nagakatsu Harada, Maiko Okuyama, Aya Yoshikatsu, Hironori Yamamoto, Saori Ishiwata, Chikako Hamada, Tomoyo Hirose, Masayuki Shono, Masashi Kuroda, Rie Tsutsumi, Jiro Takeo, Yutaka Taketani, Yutaka Nakaya and Hiroshi Sakaue :
Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism.,
Journal of Cellular Biochemistry, Vol.118, No.11, 3810-3824, 2017.

(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jcb.26031
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28383761; ● Search Scopus @ Elsevier (PMID): 28383761; ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.26031

(DOI: 10.1002/jcb.26031, PubMed: 28383761) Masato Miyake, Masashi Kuroda, Hiroshi Kiyonari, Kenji Takehana, Satoshi Hisanaga, Masatoshi Morimoto, Jun Zhang, Miho Oyadomari, Hiroshi Sakaue and Seiichi Oyadomari :
Ligand-induced rapid skeletal muscle atrophy in HSA-Fv2E-PERK transgenic mice.,
PLoS ONE, Vol.12, No.6, e0179955, 2017.

(要約): As a novel model of muscle wasting, HSA-Fv2E-PERK Tg mice provide a convenient tool for studying the pathogenesis of muscle loss and for assessing putative therapeutics.
(徳島大学機関リポジトリ): ● Metadata: 114340
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0179955
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28644884; ● Search Scopus @ Elsevier (PMID): 28644884; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0179955

(徳島大学機関リポジトリ: 114340, DOI: 10.1371/journal.pone.0179955, PubMed: 28644884) Kiyoe Kurahashi, Seika Inoue, Sumiko Yoshida, Yasumasa Ikeda, Kana Morimoto, Ryoko Uemoto, Kazue Ishikawa, Takeshi Kondo, Tomoyuki Yuasa, Itsuro Endo, Masato Miyake, Seiichi Oyadomari, Toshio Matsumoto, Masahiro Abe, Hiroshi Sakaue and Ken-ichi Aihara :
The Role of Heparin Cofactor in the Regulation of Insulin Sensitivity and Maintenance of Glucose Homeostasis in Humans and Mice.,
Journal of Atherosclerosis and Thrombosis, 2017.

(要約): The present studies provide evidence to support the idea that HC plays an important role in the maintenance of glucose homeostasis by regulating insulin sensitivity in both humans and mice. Stimulators of HC production may serve as novel therapeutic tools for the treatment of type 2 diabetes.
(徳島大学機関リポジトリ): ● Metadata: 110925
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.37739
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28502917; ● Search Scopus @ Elsevier (PMID): 28502917; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.37739

(徳島大学機関リポジトリ: 110925, DOI: 10.5551/jat.37739, PubMed: 28502917) Yutaka Nakaya, Daiju Fukuda, Takashi Oyamada, Kazuo Ogawa, Nagakatsu Harada, Hironori Nakagami, Ryuichi Morishita, Masataka Sata and Hiroshi Sakaue :
A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury.,
The Journal of Medical Investigation : JMI, Vol.64, No.1, 2, 64-67, 2017.

(要約): Although Lp(a) have been thought to be a cardiovascular risk factor, it is unclear whether lowering Lp(a) levels reduces the risk of cardiovascular diseases. No pharmacological agents which selectively reduce serum Lp(a) levels, and Lp(a) is present in primate but absent in common laboratory animals such as mice and pigs. In the present study we used transgenic mice of human Lp(a) and tested effect a novel Lp(a) lowering drug D-47 on neointima formation after vascular injury. D-47 successfully decreased plasma levels of Lp(a) and possibly inhibited neointima formation in Lp(a) transgenic mice. The results indicate that we can modulate plasma Lp(a) levels by pharmacologic agents and inhibit atherogenic properties of Lp(a) by reducing plasma levels of Lp(a). J. Med. Invest. 64: 64-67, February, 2017.
(キーワード): lipoprotein a / 動脈硬化 (atherosclerosis) / cardiovascular events / low density lipoprotein
(徳島大学機関リポジトリ): ● Metadata: 111083
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.64.64
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28373630; ● Search Scopus @ Elsevier (PMID): 28373630; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.64

(徳島大学機関リポジトリ: 111083, DOI: 10.2152/jmi.64.64, PubMed: 28373630) Yumiko Miyatake, Tetsuya Shiuchi, Kazuaki Mawatari, Satomi Toda, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Masashi Kuroda, Mayu Sebe, Rie Tsutsumi, Nagakatsu Harada, Yasuhiko Minokoshi, Tadahiro Kitamura, Koro Gotoh, Masaki Ueno, Yutaka Nakaya and Hiroshi Sakaue :
Intracerebroventricular injection of ghrelin decreases wheel running activity in rats.,
Peptides, Vol.87, 12-19, 2017.

(要約): There is an increasing interest in elucidating the molecular mechanisms by which voluntary exercise is regulated. In this study, we examined how the central nervous system regulates exercise. We used SPORTS rats, which were established in our laboratory as a highly voluntary murine exercise model. SPORTS rats showed lower levels of serum ghrelin compared with those of the parental line of Wistar rats. Intracerebroventricular and intraperitoneal injection of ghrelin decreased wheel-running activity in SPORTS rats. In addition, daily injection of the ghrelin inhibitor JMV3002 into the lateral ventricles of Wistar rats increased wheel-running activity. Co-administration of obestatin inhibited ghrelin-induced increases in food intake but did not inhibit ghrelin-induced suppression of voluntary exercise in rats. Growth hormone secretagogue receptor (GHSR) in the hypothalamus and hippocampus of SPORTS rats was not difference that in control rats. We created an arcuate nucleus destruction model by administering monosodium glutamate (MSG) to neonatal SPORTS rats. Injection of ghrelin into MSG-treated rats decreased voluntary exercise but did not increase food intake, suggesting that wheel-running activity is not controlled by the arcuate nucleus neurons that regulate feeding. These results provide new insights into the mechanism by which ghrelin regulates voluntary activity independent of arcuate nucleus neurons.
(徳島大学機関リポジトリ): ● Metadata: 113364
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.peptides.2016.11.005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27825986; ● Summary page in Scopus @ Elsevier: 2-s2.0-84995961350

(徳島大学機関リポジトリ: 113364, DOI: 10.1016/j.peptides.2016.11.005, PubMed: 27825986, Elsevier: Scopus) 堤理恵, 阪上浩, 西村匡司 :
ARDS患者に投与すべき熱量はどのように決めるのか?,
救急・集中治療,ARDS-その常識は正しいか?-, Vol.29, No.1-2, 125-1313, 2017年. Zhi-Hong Yang, Masahiro Bando, Toshihiro Sakurai, Ye Chen, Beatrice Emma-Okon, Bree Wilhite, Daiju Fukuda, Boris Vaisman, Milton Pryor, Yoshiyuki Wakabayashi, Maureen Sampson, Zu-Xi Yu, Akiko Sakurai, Abdalrahman Zarzour, Hiroko Miyahara, Jiro Takeo, Hiroshi Sakaue, Masataka Sata and Alan T. Remaley :
Long-chain monounsaturated fatty acid-rich fish oil attenuates the development of atherosclerosis in mouse models.,
Molecular Nutrition & Food Research, Vol.60, No.10, 2208-2218, 2016.

(要約): SCOPE: Fish oil-derived long-chain monounsaturated fatty acids (LCMUFA) containing chain lengths longer than 18 were previously shown to improve cardiovascular disease risk factors in mice. However, it is not known if LCMUFA also exerts anti-atherogenic effects. The main objective of the present study was to investigate the effect of LCMUFA on the development of atherosclerosis in mouse models.METHODS AND RESULTS: LDLR-KO mice were fed Western diet supplemented with 2% (w/w) of either LCMUFA concentrate, olive oil, or not (control) for 12 wk. LCMUFA, but not olive oil, significantly suppressed the development of atherosclerotic lesions and several plasma inflammatory cytokine levels, although there were no major differences in plasma lipids between the three groups. At higher doses 5% (w/w) LCMUFA supplementation was observed to reduce pro-atherogenic plasma lipoproteins and to also reduce atherosclerosis in ApoE-KO mice fed a Western diet. RNA sequencing and subsequent qPCR analyses revealed that LCMUFA upregulated PPAR signaling pathways in liver. In cell culture studies, apoB-depleted plasma from LDLR-K mice fed LCMUFA showed greater cholesterol efflux from macrophage-like THP-1 cells and ABCA1-overexpressing BHK cells.CONCLUSION: Our research showed for the first time that LCMUFA consumption protects against diet-induced atherosclerosis, possibly by upregulating the PPAR signaling pathway.
(キーワード): Long-chain monounsaturated / 動脈硬化 (atherosclerosis) / PPAR signaling / cholesterol efflux, / 炎症 (inflammation)
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/mnfr.201600142
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27273599; ● Summary page in Scopus @ Elsevier: 2-s2.0-85027917138

(DOI: 10.1002/mnfr.201600142, PubMed: 27273599, Elsevier: Scopus) Masashi Kuroda, Ayako Tominaga, Kasumi Nakagawa, Misa Nishiguchi, Mayu Sebe, Yumiko Miyatake, Tadahiro Kitamura, Rie Tsutsumi, Nagakatsu Harada, Yutaka Nakaya and Hiroshi Sakaue :
DNA Methylation Suppresses Leptin Gene in 3T3-L1 Adipocytes.,
PLoS ONE, Vol.11, No.8, e0160532, 2016.

(要約): Leptin is a key regulator of energy intake and expenditure. This peptide hormone is expressed in mouse white adipose tissue, but hardly expressed in 3T3-L1 adipocytes. Using bisulfite sequencing, we found that CpG islands in the leptin promoter are highly methylated in 3T3-L1cells. 5-azacytidine, an inhibitor of DNA methyltransferase, markedly increased leptin expression as pre-adipocytes matured into adipocytes. Remarkably, leptin expression was stimulated by insulin in adipocytes derived from precursor cells exposed to 5-azacytidine, but suppressed by thiazolidinedione and dexamethasone. In contrast, adipocytes derived from untreated precursor cells were unresponsive to both 5-azacytidine and hormonal stimuli, although lipid accumulation was sufficient to boost leptin expression in the absence of demethylation. Taken together, the results suggest that leptin expression in 3T3-L1 cells requires DNA demethylation prior to adipogenesis, transcriptional activation during adipogenesis, and lipid accumulation after adipogenesis.
(徳島大学機関リポジトリ): ● Metadata: 110107
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0160532
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27494408; ● Search Scopus @ Elsevier (PMID): 27494408; ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0160532

(徳島大学機関リポジトリ: 110107, DOI: 10.1371/journal.pone.0160532, PubMed: 27494408) Michio Shimabukuro, H Sato, Hirofumi Izaki, Daiju Fukuda, E Uematsu, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Hiro-omi Kanayama, H Masuzaki and Masataka Sata :
Depot- and gender-specific expression of NLRP3 inflammasome and toll-like receptors in adipose tissue of cancer patients.,
BioFactors, Vol.42, No.4, 397-406, 2016.

(キーワード): obesity / inflammation / gender
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/biof.1287
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27086574; ● Summary page in Scopus @ Elsevier: 2-s2.0-84982113330

(DOI: 10.1002/biof.1287, PubMed: 27086574, Elsevier: Scopus) Sachiko Nishimoto, Daiju Fukuda, Yasutomi Higashikuni, Kimie Tanaka, Yoichiro Hirata, Chie Murata, Joo-Ri Kim-Kaneyama, Fukiko Sato, Masahiro Bando, Shusuke Yagi, Takeshi Soeki, Tetsuya Hayashi, Issei Imoto, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata :
Obesity-induced DNA released from adipocytes stimulates chronic adipose tissue inflammation and insulin resistance.,
Science Advances, Vol.2, No.3, e1501332, 2016.

(要約): Obesity stimulates chronic inflammation in adipose tissue, which is associated with insulin resistance, although the underlying mechanism remains largely unknown. Here we showed that obesity-related adipocyte degeneration causes release of cell-free DNA (cfDNA), which promotes macrophage accumulation in adipose tissue via Toll-like receptor 9 (TLR9), originally known as a sensor of exogenous DNA fragments. Fat-fed obese wild-type mice showed increased release of cfDNA, as determined by the concentrations of single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) in plasma. cfDNA released from degenerated adipocytes promoted monocyte chemoattractant protein-1 (MCP-1) expression in wild-type macrophages, but not in TLR9-deficient (Tlr9 (-/-) ) macrophages. Fat-fed Tlr9 (-/-) mice demonstrated reduced macrophage accumulation and inflammation in adipose tissue and better insulin sensitivity compared with wild-type mice, whereas bone marrow reconstitution with wild-type bone marrow restored the attenuation of insulin resistance observed in fat-fed Tlr9 (-/-) mice. Administration of a TLR9 inhibitory oligonucleotide to fat-fed wild-type mice reduced the accumulation of macrophages in adipose tissue and improved insulin resistance. Furthermore, in humans, plasma ssDNA level was significantly higher in patients with computed tomography-determined visceral obesity and was associated with homeostasis model assessment of insulin resistance (HOMA-IR), which is the index of insulin resistance. Our study may provide a novel mechanism for the development of sterile inflammation in adipose tissue and a potential therapeutic target for insulin resistance.
(徳島大学機関リポジトリ): ● Metadata: 110123
(出版サイトへのリンク): ● Publication site (DOI): 10.1126/sciadv.1501332
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27051864; ● Search Scopus @ Elsevier (PMID): 27051864; ● Search Scopus @ Elsevier (DOI): 10.1126/sciadv.1501332

(徳島大学機関リポジトリ: 110123, DOI: 10.1126/sciadv.1501332, PubMed: 27051864) Sebe Mayu, Rie Tsutsumi, Yamaguchi Sotaro, Horikawa T. Yousuke, Harada Nagakatsu, Takuro Oyama, Nami Kakuta, Katsuya Tanaka, Yasuo Tsutsumi, Yutaka Nakaya and Hiroshi Sakaue :
The synergistic effects of omega-3 fatty acids against 5-fluorouracil-induced mucosal impairment in mice.,
BMC Nutrition, Vol.2, No.17, 1-10, 2016.

(徳島大学機関リポジトリ): ● Metadata: 114371
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s40795-016-0057-7
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.1186/s40795-016-0057-7

(徳島大学機関リポジトリ: 114371, DOI: 10.1186/s40795-016-0057-7) Maerjianghan Abuduli, Hirokazu Ohminami, Tamaki Otani, Hitoshi Kubo, Haruka Ueda, Yoshichika Kawai, Masashi Masuda, Hisami Okumura, Hiroshi Sakaue, Hironori Yamamoto, Eiji Takeda and Yutaka Taketani :
Effects of dietary phosphate on glucose and lipid metabolism.,
American Journal of Physiology, Endocrinology and Metabolism, Vol.310, No.7, E526-E538, 2016.

(要約): Recent epidemiological and animal studies have suggested that excess intake of phosphate (Pi) is a risk factor for the progression of chronic kidney disease and its cardiovascular complications. However, little is known about the impact of dietary high Pi intake on the development of metabolic disorders such as obesity and type II diabetes. In this study, we investigated the effects of dietary Pi on glucose and lipid metabolism in healthy rats. Male, 8-wk-old Sprague-Dawley rats were divided into 3 groups and given experimental diets containing varying amounts of Pi, i.e. 0.2% (low Pi, LP), 0.6% (control Pi, CP), and 1.2% (high Pi, HP). After 4 weeks, HP group showed lower visceral fat accumulation compared with other groups, accompanied by a low respiratory exchange ratio (VCO2/VO2) without alteration of locomotive activity. HP group had lower levels of plasma insulin and non-esterified fatty acids. In addition, HP group also showed suppressed expression of hepatic lipogenic genes including sterol regulatory element binding protein-1c, fatty acid synthase, and acetyl-CoA carboxylase, whereas there was no difference in hepatic fat oxidation among the groups. On the other hand, uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator alpha (PGC1) expression were significantly increased in the brown adipose tissue (BAT) of HP group. Our data demonstrated that a high Pi diet can negatively regulate lipid synthesis in the liver, and increased mRNA expression related to lipid oxidation and UCP1 in BAT, thereby preventing visceral fat accumulation. Thus, dietary Pi is a novel metabolic regulator.
(徳島大学機関リポジトリ): ● Metadata: 109976
(出版サイトへのリンク): ● Publication site (DOI): 10.1152/ajpendo.00234.2015
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26786774; ● Search Scopus @ Elsevier (PMID): 26786774; ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00234.2015

(徳島大学機関リポジトリ: 109976, DOI: 10.1152/ajpendo.00234.2015, PubMed: 26786774) Otsuka Ryo, Nagakatsu Harada, Aoki Shouhei, Shirai Kanna, Kazuchika Nishitsuji, Nozaki Ayane, Hatakeyama Adzumi, Masayuki Shono, Noriko Mizusawa, Katsuhiko Yoshimoto, Yutaka Nakaya, Hiroshi Kitahata and Hiroshi Sakaue :
C-terminal region of GADD34 regulates eIF2alpha dephosphorylation and cell proliferation in CHO-K1 cells.,
Cell Stress & Chaperones, Vol.21, No.1, 29-40, 2016.

(要約): GADD34 is a member of a growth arrest and DNA damage (GADD)-inducible gene family. Here, we established a novel Chinese hamster ovary (CHO)-K1-derived cell line, CHO-K1-G34M, which carries a nonsense mutation (termed the Q525X mutation) in the GADD34 gene. The Q525X mutant protein lacks the C-terminal 66 amino acids required for GADD34 to bind to and activate protein phosphatase 1 (PP1). We investigated the effects of GADD34 with or without the Q525X mutation on the phosphorylation status of PP1 target proteins, including the subunit of eukaryotic initiation factor 2 (eIF2) and glycogen synthase kinase 3 (GSK3). CHO-K1-G34M cells had higher levels of eIF2 phosphorylation compared to the control CHO-K1-normal cells both in the presence and absence of endoplasmic reticulum stress. Overexpression of the wild-type GADD34 protein in CHO-K1-normal cells largely reduced eIF2 phosphorylation, while overexpression of the Q525X mutant did not produce similar reductions. Meanwhile, neither wild type nor Q525X mutation of GADD34 affected the GSK3 phosphorylation status. GADD34 also did not affect the canonical Wnt signaling pathway downstream of GSK3. Cell proliferation rates were higher, while expression levels of the cyclin-dependent kinase inhibitor p21 were lower in CHO-K1-G34M cells compared to the CHO-K1-normal cells. The GADD34 Q525X mutant had a reduced ability to inhibit cell proliferation and enhance p21 expression of the CHO-K1-normal cells compared to the wild-type GADD34 protein. These results suggest that the GADD34 protein C-terminal plays important roles in regulating not only eIF2 dephosphorylation but also cell proliferation in CHO-K1 cells.
(徳島大学機関リポジトリ): ● Metadata: 110106
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12192-015-0633-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26318739; ● Summary page in Scopus @ Elsevier: 2-s2.0-84951905379

(徳島大学機関リポジトリ: 110106, DOI: 10.1007/s12192-015-0633-9, PubMed: 26318739, Elsevier: Scopus) Yumiko Miyatake, Tetsuya Shiuchi, Tomoyo Ueta, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Tadahiro Kitamura, Rie Tsutsumi, Nagakatsu Harada, Yutaka Nakaya and Hiroshi Sakaue :
Intracerebroventricular injection of adiponectin regulates locomotor activity in rats,
The Journal of Medical Investigation : JMI, Vol.62, No.3-4, 199-203, 2015.

(要約): Enhancing exercise motivation is the best way to prevent obesity and diabetes. In this study, we examined whether adiponectin affects locomotion activity in Wister and Spontaneously-Running Tokushima-Shikoku (SPORTS) rats using two types of behavioral assays: home cage and wheel running activity. SPORTS rats were established from an original line from Wister strain that had shown high level of wheel running activity in our laboratory. Injection of adiponectin into the lateral ventricle of Wister rats and SPORTS rats decreased home cage activity, but no change was observed in the food intake and oxygen consumption. This result indicates the possibility that adiponectin can reduce non-exercise activity thermogenesis (NEAT) and physical activity via the central nervous system. In contrast, injection of adiponectin did not change wheel running activity in SPORTS rats. We produced hypothalamus-destructed model rat using monosodium glutamate (MSG) to elucidate the regulation site of adiponectin. Injection of adiponectin into MSG-treated SPORTS rats did not change amount of home cage activity and food intake, suggesting that adiponectin action on home cage activity was in the hypothalamic area. These results suggest that adiponectin regulates locomotion activity through mediobasal hypothalamus.
(徳島大学機関リポジトリ): ● Metadata: 111279
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.62.199
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26399348; ● Summary page in Scopus @ Elsevier: 2-s2.0-84942037938

(徳島大学機関リポジトリ: 111279, DOI: 10.2152/jmi.62.199, PubMed: 26399348, Elsevier: Scopus) Rie Tsutsumi, Tomomi Yoshida, Yoshitaka Nii, Naoki Okahisa, Shinya Iwata, Masao Tsukayama, Rei Hashimoto, Yasuko Taniguchi, Hiroshi Sakaue, Toshio Hosaka, Emi Shuto and Tohru Sakai :
Sudachitin, a polymethoxylated flavone, improves glucose and lipid metabolism by increasing mitochondrial biogenesis in skeletal muscle.,
Nutrition & Metabolism, Vol.11, 32, 2014.

(要約): Obesity is a major risk factor for insulin resistance, type 2 diabetes, and stroke. Flavonoids are effective antioxidants that protect against these chronic diseases. In this study, we evaluated the effects of sudachitin, a polymethoxylated flavonoid found in the skin of the Citrus sudachi fruit, on glucose, lipid, and energy metabolism in mice with high-fat diet-induced obesity and db/db diabetic mice. In our current study, we show that sudachitin improves metabolism and stimulates mitochondrial biogenesis, thereby increasing energy expenditure and reducing weight gain. C57BL/6 J mice fed a high-fat diet (40% fat) and db/db mice fed a normal diet were treated orally with 5 mg/kg sudachitin or vehicle for 12 weeks. Following treatment, oxygen expenditure was assessed using indirect calorimetry, while glucose tolerance, insulin sensitivity, and indices of dyslipidemia were assessed by serum biochemistry. Quantitative polymerase chain reaction was used to determine the effect of sudachitin on the transcription of key metabolism-regulating genes in the skeletal muscle, liver, and white and brown adipose tissues. Primary myocytes were also prepared to examine the signaling mechanisms targeted by sudachitin in vitro. Sudachitin improved dyslipidemia, as evidenced by reduction in triglyceride and free fatty acid levels, and improved glucose tolerance and insulin resistance. It also enhanced energy expenditure and fatty acid β-oxidation by increasing mitochondrial biogenesis and function. The in vitro assay results suggest that sudachitin increased Sirt1 and PGC-1α expression in the skeletal muscle. Sudachitin may improve dyslipidemia and metabolic syndrome by improving energy metabolism. Furthermore, it also induces mitochondrial biogenesis to protect against metabolic disorders.
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/1743-7075-11-32
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25114710; ● Search Scopus @ Elsevier (PMID): 25114710; ● Search Scopus @ Elsevier (DOI): 10.1186/1743-7075-11-32

(DOI: 10.1186/1743-7075-11-32, PubMed: 25114710) Kazuaki Mawatari, Emiko Yoshioka, Satomi Toda, Sonoko Yasui, Hiroko Furukawa, Takaaki Shimohata, Takamasa Ohnishi, Masaki Morishima, Nagakatsu Harada, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya :
Enhancement of endothelial function inhibits left atrial thrombi development in an animal model of spontaneous left atrial thrombosis.,
Circulation Journal, Vol.78, No.8, 1980-1988, 2014.

(要約): Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats. They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980-1988).
(出版サイトへのリンク): ● Publication site (DOI): 10.1253/circj.CJ-13-1398
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24859498; ● Summary page in Scopus @ Elsevier: 2-s2.0-84905043629

(DOI: 10.1253/circj.CJ-13-1398, PubMed: 24859498, Elsevier: Scopus) Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yoji Hoshina, Kana Kato, Hitoshi Shirakawa, Hiroshi Sakaue, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita :
Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation.,
PLoS ONE, Vol.9, No.4, e93856, 2014.

(要約): It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue.
(キーワード): Adipocytes / Animals / Blotting, Western / Chemokine CCL2 / DNA Primers / Diabetes Mellitus, Type 2 / Gene Deletion / Glucagon-Like Peptide 1 / Glucose Tolerance Test / Hypoxia-Inducible Factor 1, alpha Subunit / Immunohistochemistry / Insulin / Mice / Mice, Knockout / Real-Time Polymerase Chain Reaction / Tumor Necrosis Factor-alpha
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0093856
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705496; ● Summary page in Scopus @ Elsevier: 2-s2.0-84899440448

(DOI: 10.1371/journal.pone.0093856, PubMed: 24705496, Elsevier: Scopus) Hirata Yoichiro, Hirotsugu Kurobe, Nishio Chika, Tanaka Kimie, Daiju Fukuda, Uematsu Etsuko, Nishimoto Sachiko, Takeshi Soeki, Nagakatsu Harada, Hiroshi Sakaue, Tetsuya Kitagawa, Michio Shimabukuro, Yutaka Nakaya and Masataka Sata :
Exendin-4, a glucagon-like peptide-1 receptor agonist, attenuates neointimal hyperplasia after vascular injury.,
European Journal of Pharmacology, Vol.699, No.1-3, 106-111, 2013.

(要約): Exendin-4 is a glucagon-like peptide-1 receptor agonist that has been used as a drug for treatment of type 2 diabetes. To investigate the effect of exendin-4 on the cardiovascular system, we investigated the impact of exendin-4 on neointimal hyperplasia of the femoral artery after vascular injury. We performed wire-mediated endovascular injury in C57BL/6 mice, followed by administration of exendin-4 24 nmol/kg/day via infusion pump. Four weeks after the injury, exendin-4 treatment significantly attenuated neointimal hyperplasia of the injured artery, although it did not affect glucose metabolism and lipid profile in wild-type mice. Immunofluorescence study revealed abundant expression of GLP-1 receptor on α-smooth muscle actin-positive cells in the injured vessel. Cell proliferation assay using rat aortic smooth muscle cells showed that exendin-4 reduced PDGF-BB induced smooth muscle cell proliferation through the cAMP/PKA pathway. Exendin-4 also inhibited TNFα production by peritoneal macrophages in response to inflammatory stimulus. Our findings indicate that a GLP-1 receptor agonist attenuated neointimal formation after vascular injury. GLP-1 receptor agonists or drugs that raise endogenous GLP-1 level might be effective in the treatment of vascular diseases.
(キーワード): Exendin-4 / GLP-1 / endovascular injury / neointimal hyperplasia / diabetes mellitus
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2012.11.057
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23220706; ● Search Scopus @ Elsevier (PMID): 23220706; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.11.057

(DOI: 10.1016/j.ejphar.2012.11.057, PubMed: 23220706) Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Hirata Yoichiro, Hirotsugu Kurobe, Maeda Norikazu, Hiroshi Sakaue, Masuzaki Hiroaki, Shimomura Iichiro and Masataka Sata :
Telmisartan ameliorates insulin sensitivity by activating the AMPK/SIRT1 pathway in skeletal muscle of obese db/db mice.,
Cardiovascular Diabetology, Vol.11, No.1, 139, 2012.

(要約): Telmisartan is a well-established angiotensin II type 1 receptor blocker that improves insulin sensitivity in animal models of obesity and insulin resistance, as well as in humans. Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) γ, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1). Here, we investigated the pathways through which telmisartan acts on skeletal muscle, in vitro as well as in vivo. Nine-week-old male db/db mice were fed a 60% high-fat diet, with orally administrated either vehicle (carboxymethyl-cellulose, CMC), 5 mg/kg telmisartan, or 5 mg/kg telmisartan and 1 mg/kg GW9662, a selective irreversible antagonist of PPARγ, for 5 weeks. Effects of telmisartan on Sirt1 mRNA, AMPK phosphorylation, and NAD+/NADH ratio were determined in C2C12 cultured myocytes. Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4. Our results indicate that telmisartan acts through a PPARγ-independent pathway, but at least partially exerts its effects by acting directly on skeletal muscle AMPK/SIRT1 pathways.
(キーワード): AMP-Activated Protein Kinases / Adipocytes / Administration, Oral / Angiotensin II Type 1 Receptor Blockers / Anilides / Animals / Benzimidazoles / Benzoates / Cell Line / Diabetes Mellitus / Diet, High-Fat / Disease Models, Animal / Dose-Response Relationship, Drug / Enzyme Activation / Fatty Acid Transport Proteins / Glucose Transporter Type 4 / Hypertrophy / Insulin / Islets of Langerhans / Male / Mice / Muscle Fibers, Skeletal / Muscle, Skeletal / NAD / Obesity / PPAR gamma / Phosphorylation / RNA, Messenger / Signal Transduction / Sirtuin 1 / Time Factors / Trans-Activators
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/1475-2840-11-139
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23137106; ● Search Scopus @ Elsevier (PMID): 23137106; ● Search Scopus @ Elsevier (DOI): 10.1186/1475-2840-11-139

(DOI: 10.1186/1475-2840-11-139, PubMed: 23137106) Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Yoichiro Hirata, Hirotsugu Kurobe, Hiroshi Sakaue, Yutaka Nakaya, Hiroaki Masuzaki and Masataka Sata :
Activation of AMPK-Sirt1 pathway by telmisartan in white adipose tissue: A possible link to anti-metabolic effects.,
European Journal of Pharmacology, Vol.692, No.1-3, 84-90, 2012.

(要約): Telmisartan exerts anti-metabolic effects beyond its angiotensin receptor blockade activities, but the mechanisms have hitherto remained elusive. We sought to elucidate the peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent and PPAR-γ-independent mechanisms underlying the anti-metabolic effects of telmisartan in white adipose tissue. Nine-week-old male C57BL/6 mice were fed with a 60% high-fat diet for 6 weeks, with 1mg/kg telmisartan or vehicle administrated orally during the last 3 weeks. 3T3-L1 adipocytes were cultured with telmisartan either with 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective irreversible antagonist of PPAR-γ, or compound C, an ATP-competitive inhibitor of AMPK. Western blotting and semiquantitative RT-PCR analysis were used to assess adiponectin, Sirt1, and AMPK levels. Lipid accumulation was assessed by Oil red O staining. The activation of transcription factor PPAR-γ2 was evaluated by using a luciferase reporter assay for mPPAR-γ2 expression plasmid vector. Treatment with telmisartan increased serum adiponectin levels in high-fat diet-fed mice concomitantly with an upregulation of adiponectin mRNA in visceral adipose tissue. In vitro telmisartan treatment dose-dependently increased adiponectin mRNA in 3T3-L1 cells; the increase was inhibited by compound C, but not by GW9662. Telmisartan increased expression of Sirt1 mRNA and Sirt1 protein as well as the phosphorylation of AMPK in 3T3-L1 cells. Telmisartan can increase adiponectin production in white adipose tissue partly via a PPAR-γ2-independent mechanism. Precise understanding of this molecular mechanism will require further investigation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2012.07.026
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22819702; ● Search Scopus @ Elsevier (PMID): 22819702; ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2012.07.026

(DOI: 10.1016/j.ejphar.2012.07.026, PubMed: 22819702) Nagakatsu Harada, Fujimoto Erika, Okuyama Maiko, Hiroshi Sakaue and Yutaka Nakaya :
Identification and functional characterization of human glycerol-3-phosphate acyltransferase 1 gene promoters.,
Biochemical and Biophysical Research Communications, Vol.423, No.1, 128-133, 2012.

(要約): Glycerol-3-phosphate acyltransferase 1 (GPAT1) acts as a rate limiting enzyme in triacylglycerol and phospholipid synthesis in mammals. GPAT1 regulates hepatic lipid accumulation associated with metabolic disorders. Here we have identified two transcriptional initiation sites and two promoters (promoter I and II) required for expression of the human GPAT1 (hGPAT1) gene. Promoter I regulates transcription of three alternative hGPAT1 mRNA variants, hGPAT1-V1, V2, and V3, while promoter II induces expression of a fourth variant, hGPAT1-V4. RT-PCR analysis and luciferase reporter assays revealed that promoter II acts in lipogenic tissues like the liver (and liver-derived HepG2 cells), whereas promoter I is differentially regulated and also acts in non-liver HeLa cells. Among liver-enriched transcription factors, HNF4α and C/EBPα slightly activated hGPAT1 promoter I, while factors including HNF1α altered promoter II activity. The lipogenic transcription factor SREBP1c greatly increased promoter II activity in HepG2 cells. The use of various truncated or mutated fragments of promoter II revealed that one sterol regulatory element-like motif and one inverted CCAAT box on promoter II contributed to the SREBP1c response. These cis-acting elements and trans-acting factors can be potential targets for manipulation of hepatic GPAT1 levels in humans.
(キーワード): Animals / Binding Sites / CCAAT-Enhancer-Binding Proteins / Exons / Glycerol-3-Phosphate O-Acyltransferase / HeLa Cells / Hep G2 Cells / Hepatocyte Nuclear Factor 4 / Humans / Introns / Liver / Mice / NIH 3T3 Cells / Promoter Regions, Genetic / RNA, Messenger / Response Elements / Sterol Regulatory Element Binding Protein 1 / Transcription, Genetic
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2012.05.094
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22634312; ● Search Scopus @ Elsevier (PMID): 22634312; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2012.05.094

(DOI: 10.1016/j.bbrc.2012.05.094, PubMed: 22634312) 阪上浩 :
運動とエネルギー消費 (特集エネルギー消費と代謝障害),
糖尿病, Vol.55, No.5, 306-308, 2012年.

(出版サイトへのリンク): ● Publication site (DOI): 10.11213/tonyobyo.55.306
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (NAID): 40019347702; ● Summary page in Scopus @ Elsevier: 2-s2.0-84862578603

(DOI: 10.11213/tonyobyo.55.306, CiNii: 40019347702, Elsevier: Scopus) Nakagawa Tadahiko, Nagakatsu Harada, Miyamoto Aiko, Kawanishi Yukiko, Yoshida Masaki, Masayuki Shono, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya :
Membrane topology of murine glycerol-3-phosphate acyltransferase 2.,
Biochemical and Biophysical Research Communications, Vol.418, No.3, 506-511, 2012.

(要約): Glycerol-3-phosphate acyltransferase (GPAT) is a rate-limiting enzyme in mammalian triacylglycerol biosynthesis. GPAT is a target for the treatment of metabolic disorders associated with high lipid accumulation. Although the molecular basis for GPAT1 activation has been investigated extensively, the activation of other isoforms, such as GPAT2, is less well understood. Here the membrane topology of the GPAT2 protein was examined using an epitope-tag-based method. Exogenously expressed GPAT2 protein was present in the membrane fraction of transformed HEK293 cells even in the presence of Na(2)CO(3) (100 mM), indicating that GPAT2 is a membrane-bound protein. Trypsin treatment of the membrane fraction degraded the N-terminal (FLAG) and C-terminal (myc-epitope) protein tags of the GPAT2 protein. Bioinformatic analysis of the GPAT2 protein sequence indicated four hydrophobic sequences as potential membrane-spanning regions (TM1-TM4). Immunoblotting of the myc-epitope tag, which was inserted between each TM region of the GPAT2 protein, showed that the amino acid sequence between TM3 and TM4 was protected from trypsin digestion. These results suggest that the GPAT2 protein has two transmembrane segments and that the N-terminal and C-terminal regions of this protein face the cytoplasm. These results also suggest that the enzymatically active motifs I-III of the GPAT2 protein face the cytosol, while motif IV is within the membrane. It is expected that the use of this topological model of GPAT2 will be essential in efforts to elucidate the molecular mechanisms of GPAT2 activity in mammalian cells.
(キーワード): Amino Acid Motifs / Animals / Cell Membrane / Cytoplasm / Glycerol-3-Phosphate O-Acyltransferase / HEK293 Cells / Humans / Mice / Molecular Sequence Data / Protein Structure, Tertiary
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2012.01.055
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22285183; ● Search Scopus @ Elsevier (PMID): 22285183; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2012.01.055

(DOI: 10.1016/j.bbrc.2012.01.055, PubMed: 22285183) 田中佑佳, 杉野博崇, 中西秀樹, 原田永勝, 阪上浩, 中屋豊 :
褥瘡患者において血清アルブミン値は栄養状態を表す良い指標か?,
日本病態栄養学会誌, Vol.14, No.1, 9-15, 2011年.

(キーワード): アルブミン / 褥瘡 / 栄養状態 / 栄養リスク / 炎症 (inflammation)
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (NAID): 10029598045

(CiNii: 10029598045) Yutaka Nakaya, Takaaki Shimohata, Sayaka Haraguchi, Toshiyuki Nakao, Jun Minaguchi, Haruo Sumitani, Nagakatsu Harada and Hiroshi Sakaue :
Severe catabolic state after an overnight fast in patients with chronic renal failure.,
Nutrition, Vol.27, No.3, 329-332, 2011.

(要約): Starvation causes more rapid development of a catabolic state in patients with liver cirrhosis than in normal subjects. Because the kidneys have a gluconeogenic activity similar to that of the liver, we tested whether patients with chronic renal failure develop a catabolic state after an overnight fast. The effect of an overnight fast on diurnal changes in respiratory quotient (RQ) was studied in 12 normal subjects and 12 patients with stable chronic renal failure. Changes in RQ in the early morning after an overnight fast were also studied in 27 patients with chronic renal failure not on dialysis. We also examined the effect on RQ of consuming a light snack in the evening before the measurements. The RQ before breakfast, but not at other times, was significantly lower in patients with renal failure than in normal subjects (0.824 ± 0.051 versus 0.868 ± 0.038, P < 0.05). This indicated that patients with renal failure had higher fat use and developed a catabolic state early in the morning. The RQ before breakfast showed significant inverse correlations with creatinine levels (r = -0.604, P < 0.001). Supplementation with a carbohydrate-rich snack in the evening resulted in a significant increase of 0.07 ± 0.04 (P < 0.05) in mean RQ in the early morning. This suggested that a late evening snack is useful for improving the catabolic state of patients with renal failure. Starvation involving an overnight fast facilitates catabolism of visceral and muscle proteins in renal failure. This suggests that nutritional management of renal failure should focus not only on the contents of a meal, but also on the timing of the meal.
(キーワード): Aged / Carbon Dioxide / Creatinine / Dietary Carbohydrates / Energy Metabolism / Fasting / Female / Humans / Kidney Failure, Chronic / Lipid Metabolism / Male / Middle Aged / Oxygen Consumption / Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.nut.2010.04.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21167682; ● Search Scopus @ Elsevier (PMID): 21167682; ● Search Scopus @ Elsevier (DOI): 10.1016/j.nut.2010.04.008

(DOI: 10.1016/j.nut.2010.04.008, PubMed: 21167682) Yohko Hirata, Toshio Hosaka, Takeo Iwata, Le Thi Kim Chung, Bayasgalan Jambaldorj, Kiyoshi Teshigawara, Nagakatsu Harada, Hiroshi Sakaue, Tohru Sakai, Katsuhiko Yoshimoto and Yutaka Nakaya :
Vimentin binds IRAP and is involved in GLUT4 vesicle trafficking.,
Biochemical and Biophysical Research Communications, Vol.405, No.1, 96-101, 2011.

(要約): Insulin-responsive aminopeptidase (IRAP) and GLUT4 are two major cargo proteins of GLUT4 storage vesicles (GSVs) that are translocated from a postendosomal storage compartment to the plasma membrane (PM) in response to insulin. The cytoplasmic region of IRAP is reportedly involved in retention of GSVs. In this study, vimentin was identified using the cytoplasmic domain of IRAP as bait. The validity of this interaction was confirmed by pull-down assays and immunoprecipitation in 3T3-L1 adipocytes. In addition, it was shown that GLUT4 translocation to the PM by insulin was decreased in vimentin-depleted adipocytes, presumably due to dispersing GSVs away from the cytoskeleton. These findings suggest that the IRAP binding protein, vimentin, plays an important role in retention of GSVs.
(キーワード): 3T3-L1 Cells / Animals / Cystinyl Aminopeptidase / Cytoplasmic Vesicles / Gene Knockdown Techniques / Glucose Transporter Type 4 / Mice / Protein Transport / Vimentin
(徳島大学機関リポジトリ): ● Metadata: 113298
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2010.12.134
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21216232; ● Search Scopus @ Elsevier (PMID): 21216232; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2010.12.134

(徳島大学機関リポジトリ: 113298, DOI: 10.1016/j.bbrc.2010.12.134, PubMed: 21216232) Masaki Yoshida, Nagakatsu Harada, Keiko Yoshida, Tadahiko Nakagawa, Takaaki Shimohata, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya :
High density lipoprotein inhibits the activation of sterol regulatory element-binding protein-1 in cultured cells.,
FEBS Letters, Vol.584, No.6, 1217-1222, 2010.

(要約): A link between cellular uptake of high density lipoprotein (HDL) and regulation of sterol regulatory element-binding protein-1 (SREBP-1) was investigated in vitro. HDL decreased nuclear SREBP-1 levels as well as SREBP-1 target gene expression in HepG2 and HEK293 cells. However, HDL did not repress an exogenously expressed, constitutively active form of SREBP-1. HDL increased cellular cholesterol levels, and cellular cholesterol depletion by methyl-beta-cyclodextrin abolished the effects of HDL. These results suggest that HDL inhibits the activation of SREBP-1 through a cholesterol-dependent mechanism, which may play an important role in regulating lipid synthetic pathways mediated by SREBP-1.
(キーワード): Acetyl-CoA Carboxylase / Animals / Cells, Cultured / Fatty Acid Synthetase Complex / Gene Expression Regulation, Enzymologic / Hep G2 Cells / Humans / Lipid Metabolism / Lipoproteins, HDL / Male / Promoter Regions, Genetic / Rats / Rats, Sprague-Dawley / Stearoyl-CoA Desaturase / Sterol Regulatory Element Binding Protein 1 / Transcriptional Activation
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.febslet.2010.02.034
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20171215; ● Summary page in Scopus @ Elsevier: 2-s2.0-77950369388

(DOI: 10.1016/j.febslet.2010.02.034, PubMed: 20171215, Elsevier: Scopus) Shintaro Yasue, Hiroaki Masuzaki, Sadanori Okada, Takako Ishii, Chisayo Kozuka, Tomohiro Tanaka, Junji Fujikura, Ken Ebihara, Kiminori Hosoda, Akemi Katsurada, Naro Ohashi, Maki Urushihara, Hiroyuki Kobori, Naoki Morimoto, Takeshi Kawazoe, Motoko Naitoh, Mitsuru Okada, Hiroshi Sakaue, Shigehiko Suzuki and Kazuwa Nakao :
Adipose tissue-specific regulation of angiotensinogen in obese humans and mice: impact of nutritional status and adipocyte hypertrophy.,
American Journal of Hypertension, Vol.23, No.4, 425-431, 2010.

(要約): BACKGROUND: The adipose tissue renin-angiotensin system (RAS) has been implicated in the pathophysiology of obesity and dysfunction of adipose tissue. However, neither regulation of angiotensinogen (AGT) expression in adipose tissue nor secretion of adipose tissue-derived AGT has been fully elucidated in humans. METHODS: Human subcutaneous abdominal adipose tissue (SAT) biopsies were performed for 46 subjects with a wide range of body mass index (BMI). Considering the mRNA level of AGT and indices of body fat mass, the amount of adipose tissue-derived AGT secretion (A-AGT-S) was estimated. Using a mouse model of obesity and weight reduction, plasma AGT levels were measured with a newly developed enzyme-linked immunosorbent assay (ELISA), and the contribution of A-AGT-S to plasma AGT levels was assessed. RESULTS: A-AGT-S was substantially increased in obese humans and the value was correlated with the plasma AGT level in mice. A-AGT-S and plasma AGT were higher in obese mice, whereas lower in mice with weight reduction. However, the AGT mRNA levels in the liver, kidney, and aorta were not altered in the mouse models. In both humans and mice, the AGT mRNA levels in mature adipocytes (MAs) were comparable to those in stromal-vascular cells. Coulter Multisizer analyses revealed that AGT mRNA levels in the MAs were inversely correlated with the average size of mature adipocytes. CONCLUSIONS: This study demonstrates that adipose tissue-derived AGT is substantially augmented in obese humans, which may contribute considerably to elevated levels of circulating AGT. Adipose tissue-specific regulation of AGT provides a novel insight into the clinical implications of adipose tissue RAS in human obesity.
(キーワード): Adipocytes / Adipose Tissue / Adult / Angiotensinogen / Animals / Aorta / Cell Enlargement / Female / Gene Expression Regulation / Humans / Kidney / Liver / Male / Mice / Mice, Inbred C57BL / Mice, Obese / Middle Aged / Nutritional Status / Obesity / RNA, Messenger / Renin
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/ajh.2009.263
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20057360; ● Search Scopus @ Elsevier (PMID): 20057360; ● Search Scopus @ Elsevier (DOI): 10.1038/ajh.2009.263

(DOI: 10.1038/ajh.2009.263, PubMed: 20057360) Chung Thi Kim Le, Toshio Hosaka, Yoshida Masaki, Nagakatsu Harada, Hiroshi Sakaue, Tohru Sakai and Yutaka Nakaya :
Exendin-4, a GLP-1 receptor agonist, directly induces adiponectin expression through protein kinase A pathway and prevents inflammatory adipokine expression.,
Biochemical and Biophysical Research Communications, Vol.390, No.3, 613-618, 2009.

(要約): Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor (GLP-1R) agonist that has been used as a drug injected subcutaneously for treatment of type 2 diabetes. Many studies have revealed molecular targets of Ex-4, but its influence on adipokines has not been determined. Our study showed that Ex-4 induced secretion of adiponectin into the culture medium of 3T3-L1 adipocytes. This effect of Ex-4 is due to increased adiponectin mRNA level through the GLP-1R. Both forskolin and 3-isobutyl-1-methylxanthine (IBMX), which may finally elevate cyclic adenosine monophosphate (cAMP) concentration, prevented the induction of adiponectin expression by Ex-4. Moreover, H89, a protein kinase A inhibitor, blocked the effect of Ex-4 on adiponectin. On the other hand, Ex-4 decreased the mRNA levels of inflammatory adipokines. The results indicate that Ex-4 directly promotes adiponectin secretion via the protein kinase A pathway in 3T3-L1 adipocytes and may ameliorate insulin resistance.
(キーワード): 1-Methyl-3-isobutylxanthine / 3T3-L1 Cells / Adipocytes / Adipokines / Adiponectin / Animals / Cyclic AMP-Dependent Protein Kinases / Forskolin / Glucagon-Like Peptide 1 / Inflammation / インスリン抵抗性 (insulin resistance) / Isoquinolines / Mice / Peptides / Phosphodiesterase Inhibitors / Protein Kinase Inhibitors / RNA, Messenger / Receptors, Glucagon / Sulfonamides / Venoms
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2009.10.015
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19850014; ● Search Scopus @ Elsevier (PMID): 19850014; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2009.10.015

(DOI: 10.1016/j.bbrc.2009.10.015, PubMed: 19850014)

MISC

研究者総覧に該当データはありませんでした。

総説・解説

黒田雅士, 阪上浩 :
脂肪細胞熱産生機構における転写因子による制御,
糖尿病・内分泌代謝科, Vol.51, No.1, 23-27, 2020年7月. 黒田雅士, 阪上浩 :
ADCY3遺伝子異常と肥満,
内分泌·糖尿病·代謝内科, Vol.48, No.3, 214-218, 2019年3月.

(キーワード): ADCY3 / Leptin / Melanocortin 4 receptor
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (NAID): 40021856391

(CiNii: 40021856391) Masashi Kuroda and Hiroshi Sakaue :
Adipocyte Death and Chronic Inflammation in Obesity,
The Journal of Medical Investigation : JMI, Vol.64, No.3,4, 193-196, Aug. 2017.

(要約): Cell death is closely linked to many diseases including cancer, neurodegenerative diseases, autoimmune diseases, and metabolic disorders. Increased adipocyte death has been reported during the development of obesity. Adipocyte death may be caused by excessive stress during obesity-related adipose tissue remodeling. Adipose tissue macrophages are key players in obesity-related inflammation and systemic insulin resistance. Accumulating evidence suggests that adipocyte death is involved in immune cell function and initiates inflammation through an interaction with macrophages; however, the precise mechanisms remain largely unknown. This review focuses on the contribution of dead cells (particularly dead adipocytes in adipose tissue) to the pathophysiological conditions associated with obesity. J. Med. Invest. 64: 193-196, August, 2017.
(キーワード): Adipocytes / Cell Death / Chronic Disease / Humans / Inflammation / Macrophages / Obesity
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.64.193
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954980; ● Search Scopus @ Elsevier (PMID): 28954980; ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.193

(DOI: 10.2152/jmi.64.193, PubMed: 28954980) 黒田雅士, 阪上浩 :
肥満・2型糖尿病におけるビタミンD・カルシウムの役割,
Clinical Calcium, Vol.26, No.3, 349-354, 2016年3月.

(要約): Obesity, induced by unhealthy lifestyle choices, could be involved in the development of chronic diseases like type 2 diabete. Obesity is largely due to the imbalance of energy intake and expenditure, therefore we have put more emphasis on the amount of macronutrients including carbohydrates, fats and proteins as dietary therapy for obesity and related-conditions. On the other hand, several studies revealed obese or diabetic patients were more likely to have micronutrient deficiencies such as vitamins and minerals. Besides the effects on bone metabolism, vitamin D and calcium might contribute to metabolic disorder accompanied by obesity. However, it has not been concluded supplementation of these two nutrients has a benefit in obese or diabetic individuals. Further studies are needed.
(キーワード): Animals / カルシウム (calcium) / Diabetes Mellitus, Type 2 / Dietary Proteins / Energy Intake / Humans / 肥満症 (obesity) / ビタミンD (vitamin D)
(出版サイトへのリンク): ● Publication site (DOI): 10.20837/4201603009
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26923970; ● Search Scopus @ Elsevier (PMID): 26923970; ● Search Scopus @ Elsevier (DOI): 10.20837/4201603009

(DOI: 10.20837/4201603009, PubMed: 26923970) 堤理恵, Yasuo M. Tsutsumi , 阪上浩 :

救急・集中治療重症患者の栄養治療, Vol.27, No.7.8, 585-590, 2015年8月. 阪上浩, 田渕正樹 :
最新臨床脳卒中学(上),
日本臨牀, Vol.72, No.5, 250-252, 2014年6月. 阪上浩, 興津理絵, 黒田雅士 :
肥満と肥満症基礎研究の進歩脂肪細胞の肥大と増殖(,
日本臨牀, Vol.72, No.4, 66-70, 2014年5月. 黒田雅士, 阪上浩 :
I. Q 6．脂肪における高血糖の急性毒性,
救急・集中治療, Vol.24, No.5-6, 545-550, 2012年6月. 阪上浩 :
栄養学からみた糖尿病・肥満研究(1),
プラクティス, Vol.28, No.6, 549-551, 2011年11月. 福田亜希子, 阪上浩 :
飽和脂肪酸とメタボの関係は? 飽和脂肪酸を摂るとメタボになりやすいですか?(動物実験の結果を含めて),
Q&Aでわかる肥満と糖尿病, Vol.10, No.6, 846-848, 2011年11月. 阪上浩 :
栄養学からみた糖尿病・肥満研究(2),
プラクティス, Vol.28, No.5, 451-453, 2011年9月. 阪上浩 :
成因と病態生理メタボリックシンドローム発症基盤としての脂肪細胞機能異常脂肪細胞分化・増殖の制御機構とその破綻,
日本臨床, Vol.69, No.1, 206-210, 2011年1月. 阪上浩 :
脂肪細胞の数と大きさの制御と病態生理的意義,
内分泌・糖尿病・代謝内科, Vol.31, No.6, 519-525, 2010年12月. 阪上浩 :
脂肪細胞数の制御機構と炎症,
糖尿病の進歩, Vol.44, 196-200, 2010年9月. 中屋豊, 原田永勝, 堤理絵, 阪上浩 :
肝硬変に対する栄養サポートのエビデンス,
静脈経腸栄養, Vol.25, No.5, 1057-1062, 2010年.

講演・発表

Masashi Kuroda, Naho Ugawa, Etsuko Ishikawa, Yasuyo Kawabata, Saya Okamoto, Waka Sasaki, Saeko Masumoto, Rie Tsutsumi and Hiroshi Sakaue :
Transcription factor IRF7 and energy metabolism,
The 11th Scientific Meeting of the Asian Association for the Study of Diabetes., May 2019. Nishimoto Sachiko, Daiju Fukuda, Higashikuni Yasutomi, Tanaka Kimie, Hirata Yoichiro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata :
Genetic deletion of TLR9 promotes blood flow recovery in hind limb ischemia,
19th International Vascular Biology Meeting, Nov. 2016. S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata :
Toll-like Receptor 9 Plays a Pivotal Role in Angiotensin II-induced Atherosclerosis.,
AHA Scientific Sessions 2015, Orlando, Nov. 2015. S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata :
The activation of toll-like receptor 9 deteriorates blood flow recovery after hind-limb ischemia.,
ESC Congress 2015, London, Aug. 2015. Taigo Horiguchi, Keiko Miyoshi, Ayako Tanimura, H. Hagita, Y. Miyatake, Hiroshi Sakaue and Takafumi Noma :
Gene expression analysis of hyperactive mutant SPORTS rat,
Cell Symposia:Exercise and Metabolism which takes place at NH Grand Krasnapolsky Hotel Amsterdam from 12-14 July 2015, Jul. 2015. S Nishimoto, Daiju Fukuda, Y Higashikuni, K Tanaka, Y Hirata, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Michio Shimabukuro and Masataka Sata :
Genetic deletion of toll-like receptor 9 accelerates blood flow recovery after hindlimb ischemia.,
AHA Scientific Sessions 2014, Chicago, Nov. 2014. Hiroshi Sakaue and 黒田雅士 :
Role of DNA methylation for leptin gene promoter in 3T3-L1 adipocytes,
Mar. 2014. Hiroshi Sakaue and 興津理恵 :
Role of the new microtubule-associated protein in the development of obesity,
国際肥満学会, Mar. 2014. S Nishimoto, Daiju Fukuda, Michio Shimabukuro, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata :
Macrophage Toll-like Receptor 9 Signaling Contributes to the Development of Insulin Resistance through the Promotion of Inflammation in Adipose Tissue.,
American Heart Association AHA 2013, Dallas, Nov. 2013. S Nishimoto, Daiju Fukuda, Michio Shimabukuro, S Matsumoto, Masayoshi Ishida, Shusuke Yagi, Takeshi Soeki, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata :
Genetic ablation of TLR9 improves insulin resistance through macrophage accumulation in adipose tissue.,
ESC Congress 2013, Amsterdam, Aug. 2013. H. Sato, Michio Shimabukuro, Y. Hirata, Hirofumi Izaki, M. Higashida, Hirotsugu Kurobe, Hiro-omi Kanayama, Hiroshi Sakaue, Yutaka Nakaya and Masataka Sata :
Region-specific regulation of the innate immune system, NLRP3 inflammasome, in human abdominal adipose tissue.,
ESC Congress 2012, Munich, Aug. 2012. Yutaka Nakaya, Shimohata Takaaki, Haraguchi Sayaka, Nakao Toshiyuki, Minaguchi Jun, Sumitani Haruo, Nagakatsu Harada and Hiroshi Sakaue :
Severe Catabolic State After An Overnight Fast In Patients With Chronic Renal Failure,
31stESPEN Congress, Wien, Aug. 2009. 阪上浩 :
エネルギー代謝に関わる末梢組織のバイオロジー白色脂肪組織のバイオロジー,
第31回日本肥満学会 2010年10月, 阪上浩 :
NSTを始めるために必要な栄養管理の知識症例に基づく経腸管理の実際,
第14会日本病態栄養学会2011年1月, 瀬部真由, 堤理恵, 瀨野浦聖佳, 岸潤, 黒田雅士, 木下成三, 中屋豊, 堤保夫, 西岡安彦, 阪上浩 :
飽和脂肪酸の過剰摂取は関節リウマチ病態の憎悪・骨格筋量の減少を引き起こす,
第23回日本病態栄養学会年次学術集会, 2020年1月. 竹治香菜, 山崎幸, 河相舞香, 松本裕華, 黒田雅士, 堤理恵, 阪上浩 :
ストレプドゾトシン抵抗性ラットにおける膵β細胞保護因子の探索,
第23回日本病態栄養学会年次学術集会, 2020年1月. 三島優奈, 堤理恵, 松本裕華, 原加奈子, 大谷環樹, 上嶋菜々子, 神田彩恵, 黒田雅士, 阪上浩 :
廃用性筋萎縮モデルにおける骨格筋・艦隊者動態の連関による生体機能制御,
第23回日本病態栄養学会年次学術集会, 2020年1月. 森万理江, 別府香名, 堤理恵, 森博康, 松久宗英, 阪上浩 :
糖尿病および透析患者における味覚障害と舌味覚受容体発言の関連について,
日本糖尿病学会中国四国地方会第57回総会, 2019年12月. 堤理恵, 瀬部真由, 岸潤, 瀨野浦聖佳, 黒田雅士, 西岡安彦, 阪上浩 :
飽和脂肪酸はインスリン抵抗性誘導を介して慢性関節リウマチを増悪させる,
第40回日本肥満学会, 2019年11月. 川端康代, 黒田雅士, 岡本彩椰, 田村優実, 富永玲奈, 堤理恵, 阪上浩 :
エネルギー代謝調節機構における転写因子IRF7の役割,
第40回日本肥満学会, 2019年11月. 竹治香菜, 山崎幸, 河相舞香, 松本裕華, 黒田雅士, 堤理恵, 阪上浩 :
ストレプトゾトシン抵抗性ラットにおける膵β細胞保護因子の探索,
第40回日本肥満学会, 2019年11月. 武田憲昭, 高岡司, 堤理恵, 阪上浩 :
難治性亜鉛欠乏性味覚障害患者に対するツイントース併用亜鉛補充療法の効果,
第32回日本口腔咽頭科学会, 2019年9月. 庄野仁志, 堤理恵, 阪上浩, 合田正和, 武田憲昭 :
シスプラチンによる舌粘膜の味覚受容体発現低下とグルコサミン酸Naの食事への添加の効果,
第32回日本口腔咽頭科学会, 2019年9月. 川端康代, 黒田雅士, 岡本彩椰, 田村優実, 富永玲奈, 堤理恵, 阪上浩 :
エネルギー代謝調節機構における転写因子IRF7の役割,
第24回アディポサイエンス・シンポジウム, 2019年8月. 山田美鈴, 黒田暁生, 堤理恵, 冨永ゆかり, 阪上浩, 松久宗英 :
循環血中遊離DNAを標的とした血管内皮細胞傷害の検出,
第62回日本糖尿病学会年次学術集会, 2019年5月. 川端康代, 黒田雅士, 宇川菜穂, 石川悦子, 岡本彩椰, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 :
肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討,
第62回日本糖尿病学会, 2019年5月. 三島優奈, 堤理恵, 宮武由実子, 末政直哉, 大谷環樹, 兒玉直子, 丹波洋介, 黒田雅士, 升本早枝子, 阪上浩 :
PET/CTを用いた代謝異常時の骨格筋における糖取り込みの測定,
第62回日本糖尿病学会, 2019年5月. 黒田雅士, 石川悦子, 宇川菜穂, 岡本彩椰, 川端康代, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 :
脂肪組織慢性炎症及びNASH病態形成における分泌タンパク質MFG-E8の関与,
第62回日本糖尿病学会, 2019年5月. 別府香名, 堤理恵, 森博康, 平野春美, 土田健司, 松久宗英, 武田憲昭, 阪上浩 :
透析患者における味覚障害と味覚受容体T1R3遺伝子の発現の関連,
第258回徳島医学会学術集会ポスターセッション, 2019年2月. 堤理恵, 山本智子, 中西信人, 阪上浩 :
敗血症における代謝破綻と血中遊離アミノ酸の意義,
日本集中治療医学会雑誌, Vol.26, No.Suppl., [O75-1], 2019年2月. 佐々木和佳, 黒田雅士, 石川悦子, 宇川菜穂, 川端康代, 升本早枝子, 堤理恵, 阪上浩 :
脱メチル化3T3-L1脂肪細胞のインスリン感受性調節因子の探索,
第39回日本肥満学会, 2018年10月. 川端康代, 黒田雅士, 石川悦子, 宇川菜穂, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 :
肥大化脂肪細胞における転写因子IRF7の同定と生理的役割の検討,
第39回日本肥満学会, 2018年10月. 黒田雅士, 阪上浩 :
肥満病態形成におけるIRF7の二つの役割,
第39回日本肥満学会, 2018年10月. 黒田雅士, 宇川菜穂, 石川悦子, 川端康代, 佐々木和佳, 升本早枝子, 堤理恵, 阪上浩 :
エネルギー代謝における転写因子IRF7の役割,
第23回アディポサイエンス・シンポジウム, 2018年8月. 宇川菜穂, 黒田雅士, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 :
肥大化脂肪細胞における転写因子 IRF7 の同定と機能解析,
第61回日本糖尿病学会, 2018年5月. 黒田雅士, 石川悦子, 宇川菜穂, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 :
脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与,
第61回日本糖尿病学会, 2018年5月. Masashi Kuroda, Etsuko Ishikawa, Naho Ugawa, Saeko Masumoto, Rie Tsutsumi, Nagakatsu Harada and Hiroshi Sakaue :
Adipose tissue-derived protein, MFG-E8, regulates chronic inflammation and obesity-related liver disease,
第91回日本内分泌学会, Apr. 2018. 井内茉莉奈, 堤理恵, 中西信人, 山本智子, 田中志歩, 大藤純, 中瀧恵実子, 小野寺睦雄, 阪上浩, 西村匡司 :
重症患者におけるエネルギー代謝動態の解析．,
第45回日本集中治療医学会学術集会, 2018年2月. 大石真実, 森博康, 鈴木麗子, 明比祐子, 黒田暁生, 田蒔基行, 谷口諭, 石津将, 阪上浩, 松久宗英 :
急速進行性糖尿病腎症に関連するリスク因子の検討,
日本糖尿病学会中国四国地方会第55回総会抄録集, 2017年11月. 堤理恵, 竹尾仁良, 板東正浩, 瀬部真由, 山﨑幸, 丹波洋介, 宮原裕子, 黒田雅士, 升本早枝子, 原田永勝, 阪上浩 :
魚油由来長鎖モノエン脂肪酸の上腕動脈内皮機能に与える効果の検討,
第38回日本肥満学会, 2017年10月. 小野山瑠美, 黒田雅士, 西口実佐, 宇川菜穂, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 :
転写制御領域解析システムを用いた3T3-L1脂肪細胞のインスリン感受性調節因子の探索,
第38回日本肥満学会, 2017年10月. 石川悦子, 黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 :
脂肪組織慢性炎症及びNASH病態形成に対するMFG-E8の関与,
第38回日本肥満学会, 2017年10月. 黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 石川悦子, 升本早枝子, 堤理恵, 原田永勝, 阪上浩 :
脂肪細胞における転写因子IRF7の同定及び機能解析,
第22回アディポサイエンス・シンポジウム, 2017年8月. 西口実佐, 黒田雅士, 小野山瑠美, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 :
肥大化脂肪細胞における転写因子IRF7の同定と機能解析,
第60回日本糖尿病学会年次学術集会, 2017年5月. 小野山瑠美, 黒田雅士, 西口実佐, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 :
3T3-L1脂肪細胞のインスリン感受性に対するDNAメチル化の制御機構,
第60回日本糖尿病学会年次学術集会, 2017年5月. 荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 倉橋清衛, 近藤剛史, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 :
1型糖尿病患者における血清IGF-1とサルコペニア罹患との関連,
第60回日本糖尿病学会年次学術集会, 2017年5月. 黒田雅士, 西口実佐, 小野山瑠美, 宇川菜穂, 堤理恵, 原田永勝, 阪上浩 :
新規肥満関連転写因子IRF7によるMCP-1発現制御機構の解析,
第90回日本内分泌学会学術集会, 2017年4月. 井内茉莉奈, 堤理恵, 中西信人, 大藤純, 中瀧恵実子, 小野寺睦雄, 阪上浩, 西村匡司 :
重症患者における栄養投与開始時期と体組成変化の関連性の検討．,
第44回日本集中治療医学会学術集会, 2017年3月. 荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 松久宗英 :
1型糖尿病患者の血清IGF-1がサルコペニア羅患に及ぼす影響,
第20回日本病態栄養学会年次学術集会, 2017年1月. 丹波洋介, 竹尾仁良, 板東正浩, 瀬部真由, 山崎幸, 福田大受, 宮原裕子, 宮武由実子, 末政直哉, 黒田雅士, 升本早枝子, 原田永勝, 堤理恵, 佐田政隆, 阪上浩 :
魚油由来長鎖モノエン脂肪酸は抗動脈硬化作用を有する,
第21回病態栄養学会年次学術集会, 2017年1月. 高橋梨恵, 宮本理人, 友川剛己, 宮武由実子, 阪上浩, 池田康将, 玉置俊晃, 土屋浩一郎 :
脳内グリコーゲンによる代謝調節効果の検討,
第130回日本薬理学会近畿部会, 2016年11月. 大石真実, 谷口諭, 明比祐子, 森博康, 玉木悠, 黒田暁生, 田蒔基行, 荒木迪子, 阪上浩, 松久宗英 :
eGFR変化量を用いた透析導入高リスク群抽出アルゴリズムの妥当性の検討,
日本糖尿病学会中国四国地方会第54回総会, 2016年11月. 荒木迪子, 森博康, 黒田暁生, 鈴木麗子, 大石真実, 谷口諭, 田蒔基行, 明比祐子, 阪上浩, 倉橋清衛, 吉田守美子, 遠藤逸朗, 粟飯原賢一, 船木真理, 松久宗英 :
1型糖尿病患者の血清IGF-1がサルコペニア罹患に及ぼす影響,
第14回1型糖尿病研究会, 2016年11月. 板東正浩, 竹尾仁良, 福田大受, 宮原裕子, 楊志宏, 西本幸子, 齋藤沙緒理, 川上真智子, 上吉原絢, 丹波洋介, 佐田政隆, 阪上浩 :
長鎖モノエン脂肪酸を含む魚油による抗動脈硬化作用,
第37回日本肥満学会, 2016年10月. 荒木迪子, 森博康, 鈴木麗子, 谷口諭, 田蒔基行, 明比祐子, 黒田暁生, 阪上浩, 松久宗英 :
1型糖尿病患者における血清IGF-1の低下とサルコペニア羅漢との関連,
第253回徳島医学会学術集会, 2016年7月. 大塚良, 原田永勝, 水澤典子, 吉本勝彦, 西辻和親, 高石和美, 中屋豊, 阪上浩, 北畑洋 :
GADD34のC末端領域を欠損したCHO-K1細胞の樹立,
第253回徳島医学会学術集会, 2016年7月. 安井苑子, 谷村真優, 松原あつみ, 堤理恵, 谷佳子, 松村晃子, 島田亜紀, 阪上浩, 武田憲昭, 濵田康弘 :
頭頸部癌化学放射線療法において治療開始時のクレアチニン身長係数が有害事象や治療中断にあたえる影響,
第31回日本静脈経腸栄養学会, 2016年2月. 井内茉莉奈, 大藤純, 堤理恵, 小野寺睦雄, 阪上浩, 今中秀光, 西村匡司 :
重症患者における栄養予後指標としての位相角の有用性．,
第43回日本集中治療医学会学術集会, 2016年2月. 西本幸子, 福田大受, 東邦康智, 田中君枝, 平田陽一郎, 八木秀介, 添木武, 阪上浩, 島袋充生, 佐田政隆 :
動脈硬化におけるマクロファージTLR9の役割,
第45回日本心脈管作動物質学会, 2016年2月. 久保みゆ, 安井苑子, 谷村真優, 松原あつみ, 堤理恵, 谷佳子, 松村晃子, 島田亜紀, 阪上浩, 武田憲昭, 濵田康弘 :
頭頸部癌化学放射線療法において治療開始時のクレアチニン身長係数が有害事象に与える影響,
第19回日本病態栄養学会, 2016年1月. 橋本怜, 島袋充生, Salim Masdan Hotimah, 原知也, 福田大受, 八木秀介, 添木武, 阪上浩, 佐田政隆 :
糖尿病性血管障害におけるPAR2シグナルの関与,
CVMW 2015, 2015年12月. 西本幸子, 福田大受, 阪上浩, 島袋充生, 佐田政隆 :
動脈硬化発症におけるマクロファージToll-like receptor 9の役割,
CVMW 2015, 2015年12月. 堀口大吾, 三好圭子, 谷村綾子, 萩田浩子, 宮武由実子, 阪上浩, 野間隆文 :
運動能が亢進したSPORTSラットの遺伝子発現解析,
第38回日本分子生物学会，第88回日本生化学会合同大会, 2015年12月. 荒木迪子, 森博康, 奥村仙示, 多々納浩, 田蒔基行, 黒田暁生, 阪上浩, 松久宗英 :
食事エネルギー密度は日本人2型糖尿病患者の肥満と関連する,
第53回日本糖尿病学会中国四国地方会米子コンベンションセンター, 2015年10月. Abuduli Maerjianghan, 大南博和, 阪上浩, 大谷環樹, 上田遥香, 武田英二, 竹谷豊 :
食事性のリンが糖代謝に及ぼす影響:PET/CT用いた解析,
第36回日本肥満学会，名古屋国際会議場，愛知県名古屋市，2015年10月2日~3日, 2015年10月. 荒木迪子, 森博康, 奥村仙示, 鞍田三貴, 福尾惠介, 田蒔基行, 黒田暁生, 阪上浩, 松久宗英 :
低エネルギー密度食が2型糖尿病患者の食行動や代謝改善に与える効果の検討,
第251回徳島医学会学術集会ポスター, 2015年8月. Michio Shimabukuro, Daiju Fukuda, H Sato, S Nishimoto, T Hara, A Takashima, Y Hirata, Hirotsugu Kurobe, Shusuke Yagi, Takeshi Soeki, Hirofumi Izaki, Hiroshi Sakaue, Tetsuya Kitagawa, Hiro-omi Kanayama and Masataka Sata :
Depot- and Gender-Specific Regulation of the Innate Immune System in Adipose Tissues: A Study from Human Biopsy Samples.,
第79回日本循環器学会学術集会, Apr. 2015. Bingzi Dong, 遠藤逸朗, 近藤剛史, 大西幸代, 阪上浩, 相澤慎一, 安倍正博, 松本俊夫 :
Interleukin-11は脂肪細胞分化を抑制する,
第88回日本内分泌学会, 2015年4月. 足立知咲, 谷佳子, 山田静恵, 西麻希, 安井苑子, 菊井聡子, 橋本脩平, 長尾紀子, 秋山真敏, 大町はる佳, 松村晃子, 阪上浩, 濵田康弘 :
神経性食欲不振症患者の体重増加とエネルギー必要量との関係,
第18回日本病態栄養学会, 2015年1月. Masayoshi Ishida, Michio Shimabukuro, Shusuke Yagi, Daiju Fukuda, Takeshi Soeki, H Sato, E Uematsu, Sachiko Matsumoto, Hiroshi Sakaue, Hirofumi Izaki, Hiro-omi Kanayama and Masataka Sata :
MicroRNA-100 Regulates Adipocytokine Expression in Subcutaneous and Visceral Adipose Tissue: An Observation from Human Biopsy Study.,
第77回日本循環器学会学術集会, Mar. 2013. 阪上浩, 福田亜希子, 阪上浩, 黒田雅士, 中屋豊 :
培養脂肪細胞でのレプチン発現はDNA脱メチル化と転写因子による活性化の2つのステップで制御されている,
日本栄養・食糧学会大会講演要旨集, Vol.66, 185, 2012年5月. 二見明香里, 阪上浩, 原田永勝, 志内哲也, 中屋豊 :
中枢神経系におけるグレリンの摂食と運動調節経路の解析,
糖尿病, Vol.55, No.Suppl.1, S-300, 2012年5月. 野村和弘, 細岡哲也, 阪上浩, 春日雅人, 小川渉 :
PGC1,
糖尿病(, Vol.55, No.Suppl.1, S-303, 2012年5月. 野村和弘, 細岡哲也, 佐々木努, 北村忠弘, 阪上浩, 春日雅人, 小川渉 :
PGC1α新規スプライシングバリアントのエネルギー代謝制御における機能の検討,
日本臨床分子医学会学術総会プログラム・抄録集, 73, 2012年4月.

(キーワード): 転写因子 (transcription factor)

富永彩子, 阪上浩, 福田亜希子, 黒田雅士, 原田永勝, 中屋豊 :
3T3-L1培養脂肪細胞でのレプチン発現はDNA脱メチル化と転写因子誘導の2つのステップで制御されている,
第32回日本肥満学会, 2011年9月. 谷口康子, 阪上浩, 戸田聡美, Uuganbayar Bold, 二見明香理, 佐藤蕗子, 原田永勝, 中屋豊 :
アディポネクチンの自発運動制御作用の検討,
第32回日本肥満学会, 2011年9月. 永礼智基, 阪上浩, 春日雅人 :
脂肪細胞における転写因子KLF15の過剰発現はSCD1発現を抑制し，インスリン分泌を増加させる,
肥満研究, Vol.17, No.Suppl, 140, 2011年9月. 中川忠彦, 原田永勝, 吉田将紀, 宮本愛子, 川西由希子, 阪上浩, 中屋豊 :
脂質合成律速酵素GPAT2の膜トポロジー解析,
第32回日本肥満学会, 2011年9月. 富永彩子, 阪上浩, 福田亜希子, 黒田雅士, 原田永勝, 中屋豊 :
3T3-L1培養脂肪細胞でのレプチン発現はDNAメチル化と転写因子による活性化の2つのステップで制御されている,
第16回アディポサイエンス研究会シンポジウム, 2011年8月. 富永彩子, 阪上浩, 福田亜希子, 原田永勝, 中屋豊 :

糖尿病, Vol.54, No.Sippl.1, S-130, 2011年4月. 谷口康子, 阪上浩, 原田永勝, 中屋豊 :
中枢神経系におけるアディポネクチンの自発運動制御作用の検討,
糖尿病, Vol.54, No.Suppl.1, S-257, 2011年4月. 片山恵梨香, 山田静恵, 松村晃子, 宇野和美, 堤理絵, 保坂利男, 阪上浩, 亀岡尚美, 大森哲郎, 中屋豊 :
外来で著明な低リン血症を示した神経性無食欲症の一例,
第14回日本病態栄養学会, 2011年1月. 東田真由子, 松村晃子, 今村有希, 宇野和美, 山田静恵, 堤理絵, 保坂利男, 阪上浩, 中屋豊 :
NST自身による血糖管理により褥瘡治療に効果をあげた一症例,
第14回日本病態栄養学会, 2011年1月. 戸田聡美, 阪上浩, 谷口康子, 原田永勝, 馬渡一諭, 中屋豊, 志内哲也, 箕越靖彦 :
自発運動制御におけるGhrelinの役割,
第14回日本病態栄養学会，神奈川県横浜市, 2011年1月. 戸田聡美, 阪上浩, 谷口康子, 原田永勝, 馬渡一諭, 中屋豊, 志内哲也 :
自発運動制御におけるGhrelinの役割,
第31回日本肥満学会, 2010年10月. 富永彩子, 永禮智基, 阪上浩, 原田永勝, 春日雅人, 中屋豊 :
3T3-L1脂肪細胞でのレプチン発現に対するDNAメチル化の関与,
第31回日本肥満学会, 2010年10月. 戸田聡美, 阪上浩, 谷口康子, 原田永勝, 馬渡一諭, 中屋豊, 志内哲也, 箕越靖彦 :
自発運動制御におけるGhrelinの役割,
3回日本糖尿病学会総会年次学術集会, 2010年5月. 戸田聡美, 阪上浩, 谷口康子, 志内哲也, 原田永勝, 馬渡一諭, 中屋豊 :
自発運動制御におけるGhrelinの役割,
第64回日本栄養・食糧学会大会, 2010年5月. 中川忠彦, 原田永勝, 吉田将紀, 宮本愛子, 川西由希子, 馬渡一諭, 髙橋章, 阪上浩, 中屋豊 :
脂質合成律速酵素グリセロール-3-リン酸アシルトランスフェラーゼ2の膜トポロジー解析,
第240回徳島医学会学術集会, 2010年2月.

研究会・報告書: Hiroyasu Mori, Akio Kuroda, Michiko Araki, Reiko Suzuki, Mami Ohishi, Satoshi Taniguchi, Motoyuki Tamaki, Yuko Akehi, Hiroshi Sakaue, Kiyoe Kurahashi, Takeshi Kondo, Sumiko Yoshida, Itsuro Endo, Ken-ichi Aihara, Makoto Funaki and Munehide Matsuhisa :
Advanced glycation end-products are a risk for muscle weakness in patients with type2 diabetes.,
American Diabetes Association 78th Scientific Sessions, Jun. 2017. 馬渡一諭, 吉岡愛美子, 戸田聡美, 大西隆仁, 原田永勝, 阪上浩, 中屋豊 :
高自発走行モデル動物SPORTS ratの左心房血栓形成と発症要因の解析,
第15回徳島臨床脈管研究会, 2013年11月. Dong Bingzi, Takeshi Kondo, Itsuro Endo, Yukiyo Ohnishi, Takashi Omatsu, Shin-ichi Yoshizawa, Hiroshi Sakaue and Toshio Matsumoto :
Interleukin-11 controls bone and adipose tissue mass by regulating osteoblastic and adipogenic differentiation,
4th Bone BioScience Meeting, Jun. 2013. 植野美彦, 関陽介, 井戸慶治, 髙木康志, 阪上浩, 生島仁史, 藤猪英樹, 白山靖彦, 田中秀治, 川田昌武, 長宗秀明, 古屋 S. 玲, 上岡麻衣子 :
令和元年度徳島大学高等教育研究センターアドミッション部門報告書,
令和元年度徳島大学高等教育研究センターアドミッション部門報告書, 2020年3月. 阪上浩 :
サイエンスマップ2008,
148, 2010年5月.

特許: 堤理恵, 阪上浩, 武田憲昭 : グルタミン酸を有効成分とする担がん患者の味覚及び/又は食欲障害の改善剤, . 堤理恵, 阪上浩 : . 堤理恵, 阪上浩 : (2018年5月), (2018年11月), 特許第2017-101459 WO2018/216715A1号 (2018年11月). 阪上浩, 堤理恵, 武田憲昭, 松島里那 : グルタミン酸を有効成分とする担がん患者の味覚及び/又は食欲障害の改善剤, 特願2016-13808 (2016年1月), .
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: 抗動脈硬化作用を有する極長鎖一価不飽和脂肪酸の基盤・応用研究 (研究課題/領域番号: 19H04055 )
転写因子IRF7による肥満・メタボリックシンドローム治療の基礎的基盤の確立 (研究課題/領域番号: 16K09753 )
末梢性シグナル分子による運動制御機構の解明 (研究課題/領域番号: 25126718 )
細胞骨格制御による肥満・メタボリックシンドローム治療の基礎的基盤の確立 (研究課題/領域番号: 24591333 )
インスリン感受性機構と脂肪酸の質との関係の解明 (研究課題/領域番号: 24500994 )
脂肪蓄積の分子基盤における脂肪細胞アポトーシス制御機構の解明 (研究課題/領域番号: 23126520 )
摂食調節因子による自発運動及びエネルギー代謝調節機構の解明 (研究課題/領域番号: 22700693 )
新規脂肪酸結合蛋白を標的分子としたメタボリックシンドローム治療の基礎的基盤の確立 (研究課題/領域番号: 21591151 )
運動習慣は自己修復細胞を活性化しうるかー脳卒中発症遅延と延命効果 (研究課題/領域番号: 20500636 )
エネルギー代謝制御機構における転写因子KLF15の生理的意義の解明 (研究課題/領域番号: 18590988 )
脂肪細胞の細胞周期制御機構を治療標的とした肥満症治療法の確立とその応用 (研究課題/領域番号: 18052012 )
細胞周期制御機構をターゲットとした新たな肥満・糖尿病治療の基盤確立とその応用 (研究課題/領域番号: 16590885 )
脂肪細胞分化を制御する自己分泌性液性因子の同定とそのシグナル伝達機構の解明 (研究課題/領域番号: 16046214 )
研究者番号（60372645）による検索

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2020年12月4日更新

専門分野・研究分野: 糖尿病・肥満
所属学会・所属協会: 社団法人日本糖尿病学会
日本肥満学会
日本病態栄養学会
社団法人日本内分泌学会
日本薬理学会
日本糖尿病・肥満動物学会
社団法人日本内科学会
米国糖尿病学会
委員歴・役員歴: 社団法人日本糖尿病学会 (評議員)
日本肥満学会 (編集委員，評議員)
日本病態栄養学会 (評議員)
受賞: 2015年8月, ESC Congress 2015 ベストポスター賞 (European Society of Cardiology)
活動: 研究者総覧に該当データはありませんでした。

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Jグローバル最終確認日: 2020/12/5 01:21
氏名（漢字）: 阪上浩
氏名（フリガナ）: サカウエヒロシ
氏名（英字）: Sakaue Hiroshi
所属機関: 徳島大学大学院教授
徳島大学糖尿病臨床・研究開発センター

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researchmap最終確認日: 2020/11/29 02:28
氏名（漢字）: 阪上浩
氏名（フリガナ）: サカウエヒロシ
氏名（英字）: Hiroshi Sakaue
プロフィール: リサーチマップAPIで取得できませんでした。
登録日時: 2018/1/25 08:21
更新日時: 2020/10/29 11:04
アバター画像URI: https://researchmap.jp/hsakaue/avatar.jpg
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所属ID: 0344000000
所属: 徳島大学大学院
部署: 医歯薬学研究部代謝栄養学分野
職名: 教授
学位: 医学博士
学位授与機関: 神戸大学
URL: https://taishaeiyo.jimdo.com/
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2020年4月4日更新

研究者番号: 60372645

所属（現在）: 2019/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 教授

所属（過去の研究課題 情報に基づく）*注記: 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
2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 教授
2014/4/1 : 徳島大学大学院, 栄養生命学教育部, 教授
2012/4/1 – 2013/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 准教授
2009/4/1 – 2011/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授
2007/4/1 – 2008/4/1 : 近畿大学, 医学部, 講師
2005/4/1 – 2006/4/1 : 神戸大学, 大学院医学系研究科, 助手
2005/4/1 : 神戸大学, 医学系研究科, 助手
2004/4/1 : 神戸大学, 大学院・医学系研究科, COE研究員

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 内科系臨床医学 / 代謝学
生物系
小区分59040:栄養学および健康科学関連

研究代表者以外

総合・新領域系 / 総合領域 / 健康・スポーツ科学 / 応用健康科学
総合・新領域系 / 総合領域 / 生活科学 / 食生活学

キーワード

研究代表者

プロテオミクス / プロテオーム解析 / マイクロアレイ解析 / アディポサイトカイン / 脂肪細胞 / KLF15 / 肥満症 / メタボリックシンドローム / 細胞周期 / CDK2 / 肥満 / ノックアウトマウス / Skp2 / 膵β細胞 / 脂肪酸結合蛋白 / 耐糖能異常 / Tubulin / トランスジェニックマウス / インスリン抵抗性 / 高脂肪食 / アポトーシス / アディポカイン / Adipocyte / Obesity / Diabetes / 糖尿病 / 微小管 / グレリン / レプチン / アディポネクチン / マイオカイン / 自発運動 / 細胞分化 / 細胞増殖 / p27^<Kip1> / 抗肥満薬 / 抗糖尿病薬 / Proliferation / Differentiation / p27Kip1 / Anti-obesity drug / Anti-diabetic drug / 転写因子 / エネルギー代謝 / 転写調節 / Adiopocyte / Metabolic syndrome / Transcription factor / IRF7 / ベージュ脂肪細胞 / UCP-1 / MCP-1 / 2型糖尿病 / 一価不飽和脂肪酸 / 動脈硬化 / 魚油

研究代表者以外

運動処方と運動療法 / 脳血管障害 / 血管内皮前駆細胞 / 血管新生 / 神経新生 / 脳卒中 / SHRSP / 運動習慣 / 神経幹細胞 / 機能回復 / 造血幹細胞 / 運動 / 血管発生 / 自発運動 / 摂食調節因子 / Ghrelin / 内臓脂肪 / 肥満 / glut4 / トランスロケーション / 細胞骨格 / 脂肪酸 / GLUT4 / 脂肪合成

研究課題研究成果共同研究者

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2019年9月30日

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生活習慣病によって脂肪組織と血管壁に生じる慢性炎症の機序の解明と新規治療法の開発（佐田政隆）

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

PET-CTを用いたサルコペニアの画期的診断法の開発を目指した研究

慢性炎症を分子基盤とした肥満・糖尿病および多臓器合併症の病態解明と治療法開発

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阪上浩