Chronic reactive oxygen species exposure inhibits glucose uptake and causes insulin resistance in C2C12 myotubes

被引：32

作者：

Ding, Hongwen ^{[1
]}

Heng, Baoli ^{[1
]}

He, Wenfang ^{[2
]}

Shi, Liping ^{[1
]}

Lai, Caiyong ^{[1
]}

Xiao, Long ^{[1
]}

Ren, Haolin ^{[1
]}

Mo, Shijie ^{[1
]}

Su, Zexuan ^{[1
]}

机构：

[1] Jinan Univ, Affiliated Hosp 1, Dept Urol, Guangzhou, Guangdong, Peoples R China

[2] Jinan Univ, Educ Ctr Micromorphol Med, Guangzhou, Guangdong, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2016年 / 478卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Insulin resistance; Reactive oxygen species; Glucose uptake; GLUT4; Akt2; C2C12; myotubes; OXIDATIVE STRESS; SKELETAL-MUSCLE; MECHANISMS;

D O I：

10.1016/j.bbrc.2016.08.028

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：

Reactive oxygen species (ROS) is an important regulator in cellular signaling transduction, and many previous studies have indicated that acute ROS stimulation improves insulin sensitivity in skeletal muscle. In the study, we found that chronic ROS treatment caused serious insulin resistance in C2C12 myotubes. Glucose uptake and consumption assay indicated that pretreatment with 80 mu M H2O2 for 2 h inhibited insulin-stimulated glucose uptake in C2C12 myotubes, and the reason for it, is that chronic H2O2 treatment decreased insulin-induced glucose transporter 4 (GLUT4) translocation from cell plasma to cell membrane. Moreover, Akt2 phosphorylation depended on insulin was reduced in C2C12 myotubes of chronic H2O2 treatment. Together, this study provides further demonstration that chronic ROS stress is associated with insulin resistance of skeletal muscle in the progression of type 2 diabetes. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：798 / 803

页数：6

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