NOX3-derived reactive oxygen species promote TNF-α-induced reductions in hepatocyte glycogen levels via a JNK pathway

被引：41

作者：

Li, Lanfang ^{[1
,2
,3
,4
]}

He, Qinghua ^{[1
,2
]}

Huang, Xiuqing ^{[1
,2
]}

Man, Yong ^{[1
,2
]}

Zhou, Yingsheng ^{[1
,2
]}

Wang, Shu ^{[1
,2
]}

Wang, Jianye ^{[1
,2
]}

Li, Jian ^{[1
,2
]}

机构：

[1] Beijing Hosp, Key Lab Geriatr, Beijing 100730, Peoples R China

[2] Beijing Inst Geriatr, Minist Hlth, Beijing 100730, Peoples R China

[3] Peking Union Med Coll, Grad Sch, Beijing 100730, Peoples R China

[4] Chinese Acad Med Sci, Grad Sch, Beijing 100730, Peoples R China

来源：

FEBS LETTERS | 2010年 / 584卷 / 05期

基金：

中国国家自然科学基金;

关键词：

TNF-alpha; Insulin resistance; HepG2; Reactive oxygen species; NADPH oxidase 3; INSULIN-RESISTANCE; OXIDATIVE STRESS; NADPH OXIDASE; NOX FAMILY; OBESITY; ACTIVATION; EXPRESSION;

D O I：

10.1016/j.febslet.2010.01.044

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

TNF-alpha-induced insulin resistance is associated with generation of reactive oxygen species (ROS). This study aims at defining the link between ROS production and hepatic insulin resistance. Treatment with TNF-alpha increased ROS generation through activating NADPH oxidase 3 (NOX3) in HepG2 hepatocytes. Down-regulation of NOX3 using siRNA prevented TNF-alpha-induced decrease of cellular glycogen. In the cells treated with TNF-alpha, there were NOX3-dependent activation of JNK, inhibition of IRS1 and phosphorylation of AKT/PKB and GSK. In conclusion, the effects of TNF-alpha on hepatic insulin resistance appear to be, at least in part, mediated by NOX3-derived ROS through a JNK pathway. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：995 / 1000

页数：6

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