Epigallocatechin-3-O-gallate (EGCG) protects the insulin sensitivity in rat L6 muscle cells exposed to dexamethasone condition

被引：94

作者：

Zhang, Z. F. ^{[1
]}

Li, Q. ^{[1
]}

Liang, J. ^{[1
]}

Dai, X. Q. ^{[1
]}

Ding, Y. ^{[1
]}

Wang, J. B. ^{[1
]}

Li, Y. ^{[1
]}

机构：

[1] Peking Univ, Sch Publ Hlth, Dept Food Hyg & Nutr, Beijing 100191, Peoples R China

来源：

PHYTOMEDICINE | 2010年 / 17卷 / 01期

关键词：

Epigallocatechin-3-O-gallate; Dexamethasone; Insulin resistance; Rat L6 muscle cells; GREEN TEA POLYPHENOL; DIABETES-MELLITUS; GLUCOSE-UPTAKE; GALLATE; INHIBITION; MODULATION; ACTIVATION; EXPRESSION; ADULTS; GLUT4;

D O I：

10.1016/j.phymed.2009.09.007

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

The tea polyphenol epigallocatechin-3-O-gallate (EGCG) displays some antidiabetic effects; however the mechanisms are incompletely understood. In the present study, the investigation of the effects of EGCG on insulin resistance was performed in rat L6 cells treated with dexamethasone. We found that dexamethasone increased Ser307 phosphorylation of insulin receptor substrate-1 (IRS-1) and reduced phosphorylation of AMPK and Akt. Furthermore, glucose uptake and glucose transporter (GLUT4) translocation were inhibited by dexamethasone. However, the treatment of EGCG improved insulin-stimulated glucose uptake by increasing GLUT4 translocation to plasma membrane. Furthermore, we also demonstrated these EGCG effects essentially depended on the AMPK and Akt activation. Together, our data suggested that EGCG inhibited dexamethasone-induced insulin resistance through AMPK and PI3K/Akt pathway. (C) 2009 Elsevier GmbH. All rights reserved.

引用

页码：14 / 18

页数：5

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