Linking mitochondrial bioenergetics to insulin resistance via redox biology

被引：247

作者：

Fisher-Wellman, Kelsey H. ^{[1
,2
]}

Neufer, P. Darrell ^{[1
,2
,3
]}

机构：

[1] E Carolina Univ, E Carolina Diabet & Obes Inst, Greenville, NC 27834 USA

[2] E Carolina Univ, Dept Kinesiol, Greenville, NC 27834 USA

[3] E Carolina Univ, Dept Physiol, Greenville, NC 27834 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2012年 / 23卷 / 03期

基金：

美国国家卫生研究院;

关键词：

SKELETAL-MUSCLE CELLS; REACTIVE OXYGEN; RECEPTOR SUBSTRATE-1; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; SUPEROXIDE-DISMUTASE; REPERFUSION INJURY; NAD(P)H OXIDASE; IN-VIVO; PHOSPHORYLATION;

D O I：

10.1016/j.tem.2011.12.008

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Chronic overnutrition and physical inactivity are major risk factors for insulin resistance and type 2 diabetes. Recent research indicates that overnutrition generates an increase in hydrogen peroxide (H2O2) emission from mitochondria, serving as a release valve to relieve the reducing pressure created by fuel overload, as well as a primary signal that ultimately decreases insulin sensitivity. H2O2 is a major input to cellular redox circuits that link to cysteine residues throughout the entire proteome to regulate cell function. Here we review the principles of mitochondrial bioenergetics and redox systems biology and offer new insight into how H2O2 emission may be linked via redox biology to the etiology of insulin resistance.

引用

收藏

页码：142 / 153

页数：12

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