What causes the insulin resistance underlying obesity?

被引:386
作者
Hardy, Olga T. [1 ,2 ]
Czech, Michael P. [1 ]
Corvera, Silvia [1 ]
机构
[1] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA
[2] Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA 01605 USA
基金
美国国家卫生研究院;
关键词
adipose tissue expandability; inflammation; insulin resistance; lipotoxicity; SUBCUTANEOUS ADIPOSE-TISSUE; BODY-MASS INDEX; SKELETAL-MUSCLE; INDUCED INFLAMMATION; FAT DEPOSITION; MORBID-OBESITY; SENSITIVITY; MICE; HYPERINSULINEMIA; PATHOGENESIS;
D O I
10.1097/MED.0b013e3283514e13
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts. Recent findings The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth. Summary Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.
引用
收藏
页码:81 / 87
页数:7
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