Inflammation and endoplasmic reticulum stress in obesity and diabetes
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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关键词：
Animals Humans Mice Adipose Tissue Endoplasmic Reticulum Inflammation Diabetes Mellitus, Type 2 Insulin Resistance Obesity JNK Mitogen-Activated Protein Kinases
DOI：
10.1038/ijo.2008.238
被引量：
年份：
2008
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