Immunity as a link between obesity and insulin resistance

被引：185
|
作者：
Kalupahana, Nishan S. [2 ,3 ]
Moustaid-Moussa, Naima [2 ,4 ,5 ]
Claycombe, Kate J. [1 ]
机构：
[1] USDA ARS, Grand Forks Human Nutr Res Ctr, Grand Forks, ND 58203 USA
[2] Univ Tennessee, Obes Res Ctr, Knoxville, TN 37996 USA
[3] Univ Peradeniya, Fac Med, Dept Physiol, Peradeniya, Sri Lanka
[4] Univ Tennessee, Dept Anim Sci, Knoxville, TN 37996 USA
[5] Univ Tennessee, UT Extens Dept Family & Consumer Sci, Knoxville, TN 37996 USA
来源：
MOLECULAR ASPECTS OF MEDICINE | 2012年 / 33卷 / 01期
关键词：
Obesity; Insulin resistance; Adipose tissue inflammation; Type-2; diabetes; ADIPOSE-TISSUE INFLAMMATION; ENDOPLASMIC-RETICULUM STRESS; NECROSIS-FACTOR-ALPHA; DIET-INDUCED OBESITY; T-CELLS; MATRIX METALLOPROTEINASES; MACROPHAGE ACCUMULATION; SKELETAL-MUSCLE; ADIPOCYTE SIZE; IKK-BETA;
D O I：
10.1016/j.mam.2011.10.011
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：
Obesity is a major public health problem in the United States and worldwide. Further, obesity is causally linked to the pathogenesis of insulin resistance, metabolic syndrome and type-2 diabetes (T2D). A chronic low-grade inflammation occurring in adipose tissue is at least in part responsible for the obesity-induced insulin resistance. This adipose tissue inflammation is characterized by changes in immune cell populations giving rise to altered adipo/cytokine profiles, which in turn induces skeletal muscle and hepatic insulin resistance. Detailed molecular mechanisms of insulin resistance, adipose tissue inflammation and the implications of these findings on therapeutic strategies are discussed in this review. Published by Elsevier Ltd.
引用
收藏
页码：26 / 34
页数：9
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