Inflammation and endoplasmic reticulum stress in obesity and diabetes

被引：0
作者：
G S Hotamisligil
机构：
[1] School of Public Health,Department of Genetics and Complex Diseases
[2] Harvard University,Department of Nutrition
[3] School of Public Health,undefined
[4] Harvard University,undefined
来源：
International Journal of Obesity | 2008年 / 32卷
关键词：
insulin resistance; protein folding; immune response; unfolded protein response (UPR); c-Jun N-terminal kinase (JNK); adipose tissue;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Obesity is associated with chronic low-grade inflammation. Inflammatory signals interfere with insulin action and disrupt metabolic homeostasis. The c-Jun N-terminal kinase (JNK) has been identified as a central mediator of insulin resistance. Recent studies showed that in obesity compromising endoplasmic reticulum (ER) function results in insulin resistance and type 2 diabetes that are dependent on JNK activation. In contrast, enhancing ER function in transgenic mice or by the use of chemical chaperones protects against diet-induced insulin resistance. Hence, ER stress and the related signaling networks present a critical mechanism underlying obesity-induced JNK activity, inflammatory response and insulin resistance.
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页码：S52 / S54
相关论文
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