Improving Metabolism by Throwing Out All the JNK

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Science  11 Jan 2013:
Vol. 339, Issue 6116, pp. 147-148
DOI: 10.1126/science.1233223

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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.