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Inflammation and the IKKβ/IκB/NF-κB axis in obesity- and diet-induced insulin resistance

Inflammation and the IKKβ/IκB/NF-κB axis in obesity- and diet-induced insulin resistance Antidiabetic effects associated with salicylates have been known for years, although the underlying mechanisms were not understood. We have been reinvestigating these effects in the light of recent discoveries in the areas of signal transduction and insulin resistance. Our findings showed that signaling pathways leading to IκB kinase β (IKKβ) and NF-κB are activated in insulin-responsive tissues of obese and high-fat-fed animals. Since activation correlates with the development of insulin resistance, we asked whether signaling through this might be involved in the pathogenesis of insulin resistance. Heterozygous gene deletion (Ikkβ+/−) or salicylates, working as IKKβ inhibitors, improved insulin sensitivity in insulin-resistant rodent models. Furthermore, high doses of salicylates (aspirin or salicylate) improved insulin sensitivity in patients with type II diabetes. Our studies implicate an inflammatory process in the pathogenesis of insulin resistance in obesity and type II diabetes mellitus and identify the IKKβ/NF-κB pathway as a molecular mediator of insulin resistance and pharmacological target for insulin sensitization. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Obesity Springer Journals

Inflammation and the IKKβ/IκB/NF-κB axis in obesity- and diet-induced insulin resistance

Shoelson, S E; Lee, J; Yuan, M
International Journal of Obesity , Volume 27 (3) – Nov 14, 2003
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References (17)

Publisher
Springer Journals
Copyright
Copyright © 2003 by Nature Publishing Group
Subject
Medicine & Public Health; Medicine/Public Health, general; Public Health; Epidemiology; Internal Medicine; Metabolic Diseases; Health Promotion and Disease Prevention
ISSN
0307-0565
eISSN
1476-5497
DOI
10.1038/sj.ijo.0802501
Publisher site
See Article on Publisher Site

Abstract

Antidiabetic effects associated with salicylates have been known for years, although the underlying mechanisms were not understood. We have been reinvestigating these effects in the light of recent discoveries in the areas of signal transduction and insulin resistance. Our findings showed that signaling pathways leading to IκB kinase β (IKKβ) and NF-κB are activated in insulin-responsive tissues of obese and high-fat-fed animals. Since activation correlates with the development of insulin resistance, we asked whether signaling through this might be involved in the pathogenesis of insulin resistance. Heterozygous gene deletion (Ikkβ+/−) or salicylates, working as IKKβ inhibitors, improved insulin sensitivity in insulin-resistant rodent models. Furthermore, high doses of salicylates (aspirin or salicylate) improved insulin sensitivity in patients with type II diabetes. Our studies implicate an inflammatory process in the pathogenesis of insulin resistance in obesity and type II diabetes mellitus and identify the IKKβ/NF-κB pathway as a molecular mediator of insulin resistance and pharmacological target for insulin sensitization.

Journal

International Journal of Obesity – Springer Journals

Published: Nov 14, 2003

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