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Glycaemia and body weight are regulated by sodium-glucose cotransporter 1 (SGLT1) expression via O-GlcNAcylation in the intestine.
http://hdl.handle.net/10422/00013235
http://hdl.handle.net/10422/0001323590ddcffb-fc06-4dd9-8e09-98c9e77fa655
名前 / ファイル | ライセンス | アクション |
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fendo.2020.00214 (728.1 kB)
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This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/). |
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2022-03-16 | |||||
タイトル | ||||||
タイトル | Glycaemia and body weight are regulated by sodium-glucose cotransporter 1 (SGLT1) expression via O-GlcNAcylation in the intestine. | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | GLP-1 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Glucose absorption | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Intestine | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | O-GlcNAcylation | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | SGLT1 | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
NISHIMURA, Kimihiro
× NISHIMURA, Kimihiro× FUJITA, Yukihiro× IDA, Shogo× YANAGIMACHI, Tsuyoshi× Ohashi, Natsuko× NISHI, Kiyoto× NISHIDA, Atsushi× IWASAKI, Yasumasa× MORINO, Katsutaro× UGI, Satoshi× NISHI, Eiichiro× ANDOH, Akira× MAEGAWA, Hiroshi |
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著者別名 |
西村, 公宏
× 西村, 公宏× 藤田, 征弘× 井田, 昌吾× 柳町, 剛司× 大橋, 夏子× 西, 清人× 西田, 淳史× 森野, 勝太郎× 卯木, 智× 西, 英一郎× 安藤, 朗× 前川, 聡 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Objective: The intestine is an important organ for nutrient metabolism via absorption and endocrine systems. Nutrients regulate O-GlcNAcylation, a post-translational modification of various proteins by O-GlcNAc transferase (OGT). We have previously shown that general OGT knockout induced severe weight loss and hypoglycaemia in mice, but little is known about how O-GlcNAcylation in the intestine modulates nutrient metabolism, especially glucose metabolism, through absorption. We aimed to reveal the roles of O-GlcNAcylation in glucose absorption by the small intestine and elucidate the mechanism by which O-GlcNAcylation regulates sodium-glucose cotransporter 1 (SGLT1) expression. |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Methods: First, we fasted normal mice and examined the changes in glucose transporters and O-GlcNAcylation in the intestine. Then, we generated two lines of small intestine-specific OGT-deficient mice (congenital: Ogt-VKO, tamoxifen-inducible: Ogt-iVKO) and observed the changes in body weight and in glucose and lipid metabolism. Finally, we investigated Sglt1 gene regulation by O-GlcNAcylation using enteroendocrine STC-1 cells. |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Results: Fasting decreased O-GlcNAcylation in the intestinal epithelium of normal mice. The Ogt-VKO mice showed significantly lower non-fasted blood glucose levels and were underweight compared with litter matched controls. Glycaemic excursion in the Ogt-VKO mice was significantly lower during the oral glucose tolerance test but comparable during the intraperitoneal glucose tolerance test. Furthermore, the Ogt-VKO mice exhibited lower Sglt1 expression in the small intestine compared with the control mice. We obtained similar results using the Ogt-iVKO mice only after tamoxifen administration. The oral d-xylose administration test revealed that the intestinal sugar absorption was diminished in the Ogt-iVKO mice and that GLP-1 secretion did not sufficiently increase after glucose gavage in the Ogt-iVKO mice. When using STC-1 cells, O-GlcNAcylation increased Sglt1 mRNA via a PKA/CREB-dependent pathway. |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Conclusion: Collectively, loss of O-GlcNAcylation in the intestine reduced glucose absorption via suppression of SGLT1 expression; this may lead to new treatments for malabsorption, obesity and diabetes. |
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書誌情報 |
en : Molecular Metabolism 巻 59, 発行日 2022-02-19 |
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出版者 | ||||||
出版者 | Elsevier GmbH | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2212-8778 | |||||
PMID | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | 35189429 | |||||
PMCID | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.ncbi.nlm.nih.gov/pmc/articles/pmc8902621/ | |||||
関連名称 | PMC8902621 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1016/j.molmet.2022.101458 | |||||
関連名称 | 10.1016/j.molmet.2022.101458 | |||||
権利 | ||||||
権利情報 | © 2022 The Author(s). Published by Elsevier GmbH.. All rights reserved. | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | ||||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
資源タイプ | ||||||
内容記述タイプ | Other | |||||
内容記述 | Journal Article |