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Int J Obes (Lond). 2008 Dec;32 Suppl 7:S52-4. doi: 10.1038/ijo.2008.238.

Inflammation and endoplasmic reticulum stress in obesity and diabetes.

Author information

  • Department of Genetics and Complex Diseases, School of Public Health, Harvard University, Boston, MA, USA. ghotamis@hsph.harvard.edu

Abstract

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.

PMID:
19136991
[PubMed - indexed for MEDLINE]
PMCID:
PMC2885768
Free PMC Article
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