Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance

被引：17
作者：
Lee, Jae Man [1 ,2 ]
机构：
[1] Kyungpook Natl Univ, Sch Med, Cell & Matrix Res Inst, Dept Biochem & Cell Biol, Daegu, South Korea
[2] Kyungpook Natl Univ, Sch Med, Dept Biomed Sci, Plus KNU Biomed Convergence Program BK21, Daegu, South Korea
来源：
DIABETES & METABOLISM JOURNAL | 2017年 / 41卷 / 01期
关键词：
Diabetes mellitus; type; 2; Endoplasmic reticulum stress; Hepatic steatosis; Insulin resistance; Receptors; cytoplasmic and nuclear; Unfolded protein response; UNFOLDED PROTEIN RESPONSE; BOUND TRANSCRIPTION FACTOR; ER STRESS; MICE; GLUCONEOGENESIS; ACTIVATION; STEATOSIS; PATHWAY; CLEAVAGE; OBESITY;
D O I：
10.4093/dmj.2017.41.1.10
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Chronic endoplasmic reticulum (ER) stress culminating in proteotoxicity contributes to the development of insulin resistance and progression to type 2 diabetes mellitus. Pharmacologic interventions targeting several different nuclear receptors have emerged as potential treatments for insulin resistance. The mechanistic basis for these antidiabetic effects has primarily been attributed to multiple metabolic and inflammatory functions. Here we review recent advances in our understanding of the association of ER stress with insulin resistance and the role of nuclear receptors in promoting ER stress resolution and improving insulin resistance in the liver.
引用
收藏
页码：10 / 19
页数：10
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