A central role for JNK in obesity and insulin resistance

Jiro Hirosumi, Gürol Tuncman, Lufen Chang, Cem Z. Görgün, K. Teoman Uysal, Kazuhisa Maeda, Michael Karin and Gökhan S. Hotamisligil ()
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Jiro Hirosumi: Harvard School of Public Health
Gürol Tuncman: Harvard School of Public Health
Lufen Chang: University of California , School of Medicine
Cem Z. Görgün: Harvard School of Public Health
K. Teoman Uysal: Harvard School of Public Health
Kazuhisa Maeda: Harvard School of Public Health
Michael Karin: University of California , School of Medicine
Gökhan S. Hotamisligil: Harvard School of Public Health

Nature, 2002, vol. 420, issue 6913, 333-336

Abstract: Abstract Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus, yet the molecular mechanisms of this association are poorly understood1. The c-Jun amino-terminal kinases (JNKs) can interfere with insulin action in cultured cells2 and are activated by inflammatory cytokines and free fatty acids, molecules that have been implicated in the development of type 2 diabetes3,4. Here we show that JNK activity is abnormally elevated in obesity. Furthermore, an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity. Thus, JNK is a crucial mediator of obesity and insulin resistance and a potential target for therapeutics.

Date: 2002
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DOI: 10.1038/nature01137

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