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

• DOI: 10.1126/science.1227568
• Publication Date: 2012-12-07T06:41:31Z
• Authors: Myoung Sook Han; Dae Young Jung; Caroline Morel; Saquib A. Lakhani; Jason K. Kim; Richard A. Flavell; Roger J. Davis
• Keywords: 0301 basic medicine; MAP Kinase Signaling System; 610; Diet, High-Fat; Biochemistry; Immunophenotyping; Islets of Langerhans; Mice; 03 medical and health sciences; Endocrinology; Animals; Mitogen-Activated Protein Kinase 9; Mitogen-Activated Protein Kinase 8; Obesity; Molecular Biology; Inflammation; 2. Zero hunger; Macrophages; Immunity; Cell Biology; Macrophage Activation; 3. Good health; Cellular and Molecular Physiology; Adipose Tissue; Glucose Clamp Technique; Insulin Resistance

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.