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
AUTHORS (7)
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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