Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Logo for

Science 339 (6116): 147-148

Copyright © 2013 by the American Association for the Advancement of Science

Improving Metabolism by Throwing Out All the JNK

Anthony W. Ferrante, Jr.

Obesity activates a complex immune response that includes the production of proinflammatory molecules and the recruitment of immune cells to key metabolic organs including adipose tissue (1, 2), liver (3), pancreas (4), and hypothalamus (5). This response has been implicated in derangements of local tissue metabolism and the subsequent development of obesity-associated disorders—especially type 2 diabetes, nonalcoholic fatty liver disease, and dyslipidemia. Defining regulators of obesity-induced activation of the proinflammatory response remains a challenge that offers the potential to identify therapeutic strategies to treat several metabolic diseases. On page 218 of this issue, Han et al. (6) have established that signaling by the enzymes c-Jun NH2-terminal kinases (JNK1 and JNK2) in myeloid cells is required for obesity-induced immune cell recruitment, inflammation in adipose tissue, and the development of insulin resistance and impaired glucose homeostasis.

Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, 1150 Saint Nicholas Avenue, New York, NY 10032, USA.

E-mail: awf7{at}columbia.edu



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882