Endoplasmic reticulum stress, obesity and diabetes

被引：524

作者：

Cnop, Miriam ^{[1
,2
]}

Foufelle, Fabienne ^{[3
]}

Velloso, Licio A. ^{[4
]}

机构：

[1] Univ Libre Brussels, Expt Med Lab, B-1070 Brussels, Belgium

[2] Erasmus Hosp, Div Endocrinol, B-1070 Brussels, Belgium

[3] Univ Paris 06, INSERM, UMR S 872, Ctr Rech Cordeliers, Paris, France

[4] Univ Estadual Campinas, Lab Cell Signaling, BR-13084761 Campinas, SP, Brazil

来源：

TRENDS IN MOLECULAR MEDICINE | 2012年 / 18卷 / 01期

基金：

巴西圣保罗研究基金会;

关键词：

UNFOLDED PROTEIN RESPONSE; PANCREATIC BETA-CELLS; SATURATED FATTY-ACIDS; TRANSCRIPTION FACTOR XBP1; STEAROYL-COA DESATURASE; ER STRESS; INSULIN-RESISTANCE; SKELETAL-MUSCLE; HEPATIC STEATOSIS; DOWN-REGULATION;

D O I：

10.1016/j.molmed.2011.07.010

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：

The endoplasmic reticulum (ER) stress response, also commonly known as the unfolded protein response (UPR), is an adaptive response used to align ER functional capacity with demand. It is activated in various tissues under conditions related to obesity and type 2 diabetes. Hypothalamic ER stress contributes to inflammation and leptin/insulin resistance. Hepatic ER stress contributes to the development of steatosis and insulin resistance, and components of the UPR regulate liver lipid metabolism. ER stress in enlarged fat tissues induces inflammation and modifies adipokine secretion, and saturated fats cause ER stress in muscle. Finally, prolonged ER stress impairs insulin synthesis and causes pancreatic beta cell apoptosis. In this review, we discuss ways in which ER stress operates as a common molecular pathway in the pathogenesis of obesity and diabetes.

引用

页码：59 / 68

页数：10

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