JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation

Author:

Han Myoung Sook12,Jung Dae Young2,Morel Caroline12,Lakhani Saquib A.3,Kim Jason K.24,Flavell Richard A.3,Davis Roger J.12

Affiliation:

1. Howard Hughes Medical Institute, Worcester, MA 01605, USA.

2. Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

3. Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CN 06520, USA.

4. Department of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Abstract

Macrophage JNK in Metabolic Disease Inflammation is thought to be an important driver of diet-induced obesity and insulin resistance. Proinflammatory, M1 phenotype macrophages and the c-jun NH 2 terminal kinases (JNK) are central players in this process. But whether JNK expression is specifically required inside macrophages is unclear. In mice containing a macrophage-specific deletion in both Jnk1 and Jnk2 , Han et al. (p. 218 , published online 6 December; see the Perspective by Ferrante Jr. ) 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.

Funder

National Institutes of Health

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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