Nuclear Mechanisms of Insulin Resistance

被引：88

作者：

Kang, Sona ^{[1
,2
,3
]}

Tsai, Linus T-Y. ^{[1
,2
]}

Rosen, Evan D. ^{[1
,2
]}

机构：

[1] Beth Israel Deaconess Med Ctr, Div Endocrinol, Boston, MA 02215 USA

[2] Harvard Univ, Sch Med, Boston, MA USA

[3] Univ Calif Berkeley, Dept Nutr Sci & Toxicol, Berkeley, CA 94720 USA

来源：

TRENDS IN CELL BIOLOGY | 2016年 / 26卷 / 05期

关键词：

TRANSCRIPTION FACTOR FOXO1; ACTIVATED-RECEPTOR-GAMMA; PPAR-GAMMA; GLUCOCORTICOID-RECEPTOR; ADIPOSE-TISSUE; HEPATIC GLUCONEOGENESIS; OXIDATIVE STRESS; SKELETAL-MUSCLE; ANTIDIABETIC ACTIONS; BETA-CATENIN;

D O I：

10.1016/j.tcb.2016.01.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Insulin resistance is a sine qua non of type 2 diabetes and is associated with many other clinical conditions. Decades of research into mechanisms underlying insulin resistance have mostly focused on problems in insulin signal transduction and other mitochondria! and cytosolic pathways. By contrast, relatively little attention has been focused on transcriptional and epigenetic contributors to insulin resistance, despite strong evidence that such nuclear mechanisms play a major role in the etiopathogenesis of this condition. In this review, we summarize the evidence for nuclear mechanisms of insulin resistance, focusing on three transcription factors with a major impact on insulin action in liver, muscle, and fat.

引用

页码：341 / 351

页数：11

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