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SGLT2 Inhibition by Empagliflozin Promotes Fat Utilization and Browning and Attenuates Inflammation and Insulin Resistance by Polarizing M2 Macrophages in Diet-induced Obese Mice.
https://doi.org/10.24517/00050482
https://doi.org/10.24517/00050482a02f77dd-2866-4731-96a0-a9f6b9bdd870
名前 / ファイル | ライセンス | アクション |
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ME-PR-NAGATA-N-137.pdf (3.0 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-04-06 | |||||
タイトル | ||||||
タイトル | SGLT2 Inhibition by Empagliflozin Promotes Fat Utilization and Browning and Attenuates Inflammation and Insulin Resistance by Polarizing M2 Macrophages in Diet-induced Obese Mice. | |||||
言語 | ||||||
言語 | eng | |||||
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 | |||||
ID登録 | ||||||
ID登録 | 10.24517/00050482 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Xu, Liang
× Xu, Liang× Nagata, Naoto× Nagashimada, Mayumi× Zhuge, Fen× Ni, Yinhua× Chen, Guanliang× Mayoux, Eric× Kaneko, Shuichi× Ota, Tsuguhito |
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著者別表示 |
長田, 直人
× 長田, 直人× 金子, 周一× 太田, 嗣人 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
EBioMedicine 巻 20, p. 137-149, 発行日 2017-07 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2352-3964 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.ebiom.2017.05.028 | |||||
出版者 | ||||||
出版者 | Elsevier | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Sodium-glucose cotransporter (SGLT) 2 inhibitors increase urinary glucose excretion (UGE), leading to blood glucose reductions and weight loss. However, the impacts of SGLT2 inhibition on energy homeostasis and obesity-induced insulin resistance are less well known. Here, we show that empagliflozin, a SGLT2 inhibitor, enhanced energy expenditure and attenuated inflammation and insulin resistance in high-fat-diet-induced obese (DIO) mice. C57BL/6J mice were pair-fed a high-fat diet (HFD) or a HFD with empagliflozin for 16 weeks. Empagliflozin administration increased UGE in the DIO mice, whereas it suppressed HFD-induced weight gain, insulin resistance, and hepatic steatosis. Moreover, empagliflozin shifted energy metabolism towards fat utilization, elevated AMP-activated protein kinase and acetyl-CoA carbolxylase phosphorylation in skeletal muscle, and increased hepatic and plasma fibroblast growth factor 21 levels. Importantly, empagliflozin increased energy expenditure, heat production, and the expression of uncoupling protein 1 in brown fat and in inguinal and epididymal white adipose tissue (WAT). Furthermore, empagliflozin reduced M1-polarized macrophage accumulation while inducing the anti-inflammatory M2 phenotype of macrophages within WAT and liver, lowering plasma TNFα levels and attenuating obesity-related chronic inflammation. Thus, empagliflozin suppressed weight gain by enhancing fat utilization and browning and attenuated obesity-induced inflammation and insulin resistance by polarizing M2 macrophages in WAT and liver. | |||||
権利 | ||||||
権利情報 | Copyright © Elsevier (CC-BY-NC-ND) | |||||
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 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.elsevier.com/locate/issn/23523964 | |||||
関連名称 | http://www.elsevier.com/locate/issn/23523964 |