JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation
Authors
Han, Myoung SoukJung, Dae Young
Morel, Caroline
Lakhani, Saquib A.
Kim, Jason K.
Flavell, Richard A.
Davis, Roger J.
UMass Chan Affiliations
Department of Medicine, Division of Endocrinology, Metabolism and DiabetesProgram in Molecular Medicine
Document Type
Journal ArticlePublication Date
2013-01-11Keywords
BiochemistryCell Biology
Cellular and Molecular Physiology
Endocrinology
Immunity
Molecular Biology
Metadata
Show full item recordAbstract
The cJun NH(2)-terminal kinase (JNK) signaling pathway contributes to inflammation and plays a key role in the metabolic response to obesity, including insulin resistance. Macrophages are implicated in this process. To test the role of JNK, we established mice with selective JNK deficiency in macrophages. We report that feeding a high-fat diet to control and JNK-deficient mice caused similar obesity, but only mice with JNK-deficient macrophages remained insulin-sensitive. The protection of mice with macrophage-specific JNK deficiency against insulin resistance was associated with reduced tissue infiltration by macrophages. Immunophenotyping demonstrated that JNK was required for pro-inflammatory macrophage polarization. These studies demonstrate that JNK in macrophages is required for the establishment of obesity-induced insulin resistance and inflammation.Source
Science. 2013 Jan 11;339(6116):218-22. doi: 10.1126/science.1227568. Link to article on publisher's siteDOI
10.1126/science.1227568Permanent Link to this Item
http://hdl.handle.net/20.500.14038/29862PubMed ID
23223452Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1126/science.1227568