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Sci. Signal., 15 January 2013
Vol. 6, Issue 258, p. ec11
[DOI: 10.1126/scisignal.2003955]


Physiology Macrophage JNK in Metabolic Disease

Kristen L. Mueller

Science, AAAS, Washington, DC 20005, USA

Inflammation is thought to be an important driver of diet-induced obesity and insulin resistance. Proinflammatory, M1 phenotype macrophages and the c-Jun N-terminal kinases (JNK) are central players in this process. But whether JNK is specifically required inside macrophages is unclear. In mice containing a macrophage-specific deletion in both Jnk1 and Jnk2, Han et al. (see the Perspective by Ferrante) found that the mice were protected against many of the diet-induced metabolic changes, including insulin resistance, despite similar weight gain as control mice on a high-fat diet. This protection was associated with a decrease in the presence of M1 macrophages in adipose tissue.

M. S. Han, D. Y. Jung, C. Morel, S. A. Lakhani, J. K. Kim, R. A. Flavell, R. J. Davis, JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation. Science 339, 218–222 (2013).[Abstract] [Full Text]

A. W. Ferrante Jr., Improving metabolism by throwing out all the JNK. Science 339, 147–148 (2013).[Abstract] [Full Text]

Citation: K. L. Mueller, Macrophage JNK in Metabolic Disease. Sci. Signal. 6, ec11 (2013).

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