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

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
DOI: 10.1126/science.1227568 Publication Date: 2012-12-07T06:41:31Z
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.
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