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Review
. 2008 Dec;32 Suppl 7(Suppl 7):S52-4.
doi: 10.1038/ijo.2008.238.

Inflammation and endoplasmic reticulum stress in obesity and diabetes

G S Hotamisligil  1
Affiliations
Review

Inflammation and endoplasmic reticulum stress in obesity and diabetes

G S Hotamisligil. Int J Obes (Lond). 2008 Dec.

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.

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References

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