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JNK1 and IKKbeta: molecular links between obesity and metabolic dysfunction.

Journal article
Authors Giovanni Solinas
Michael Karin
Published in FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volume 24
Issue 8
Pages 2596-611
ISSN 1530-6860
Publication year 2010
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 2596-611
Language en
Links dx.doi.org/10.1096/fj.09-151340
Keywords Humans, I-kappa B Kinase, physiology, Inflammation, Metabolic Diseases, etiology, Mitogen-Activated Protein Kinase 8, physiology, Obesity, complications, etiology, pathology
Subject categories Basic Medicine

Abstract

Inflammation is thought to underlie the pathogenesis of many chronic diseases. It is now established that obesity results in a state of chronic low-grade inflammation thought to contribute to several metabolic disorders, including insulin resistance and pancreatic islet dysfunction. The protein kinases JNK1 and IKKbeta have been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. The precise mechanisms of these linkages are still being investigated. However, as we discuss here, JNK1 and IKKbeta are activated by almost all forms of metabolic stress that have been implicated in insulin resistance or islet dysfunction. Furthermore, both JNK1 and IKKbeta are critically involved in the promotion of diet-induced obesity, metabolic inflammation, insulin resistance, and beta-cell dysfunction. Understanding the molecular mechanisms by which JNK1 and IKKbeta mediate obesity-induced metabolic stress is likely to be of importance for the development of new treatments for a variety of obesity-associated diseases.

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