Journal
INTERNATIONAL JOURNAL OF OBESITY
Volume 32, Issue -, Pages S52-S54Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ijo.2008.238
Keywords
insulin resistance; protein folding; immune response; unfolded protein response (UPR); c-Jun N-terminal kinase (JNK); adipose tissue
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Funding
- NIDDK NIH HHS [R01 DK052539, R01 DK052539-12, R01 DK064360, R01 DK064360-07] Funding Source: Medline
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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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