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Inflammation and endoplasmic reticulum stress in obesity and diabetes

International Journal of Obesity volume 32, pages S52–S54 (2008)Cite this article

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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Acknowledgements

I am grateful for the contribution of fellows and students to the studies presented here. The research programs in Hotamisligil laboratory are supported by grants from the National Institutes of Health USA, American Diabetes Association and Juvenile Diabetes Research Foundation.

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Authors and Affiliations

  1. Department of Genetics and Complex Diseases, School of Public Health, Harvard University, Boston, MA, USA

    G S Hotamisligil

  2. Department of Nutrition, School of Public Health, Harvard University, Boston, MA, USA

    G S Hotamisligil

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  1. G S Hotamisligil
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Correspondence to G S Hotamisligil.

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Conflict of interest

Gokhan S Hotamisligil has received lecture fees from Merck, Schering Plough, Pfizer and Glaxo Smith Kline and is a member of the SAB of Lipomics Technologies Inc. and Syndexa Pharmaceuticals. In addition, Gokhan S Hotamisligil owns stock options with Lipomics Technologies Inc. and Syndexa Pharmaceuticals and has received grant support from Syndexa.

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Hotamisligil, G. Inflammation and endoplasmic reticulum stress in obesity and diabetes. Int J Obes 32 (Suppl 7), S52–S54 (2008). https://doi.org/10.1038/ijo.2008.238

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