JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation
Howard Hughes Medical Institute · University of Massachusetts Chan Medical School
Abstract
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…
Citation impact
- FWCI
- 30.07
- Percentile
- 100%
- References
- 33
Authors
7- MSMyoung Sook Han
Howard Hughes Medical Institute, University of Massachusetts Chan Medical School
- DYDae Young Jung
University of Massachusetts Chan Medical School
- CMCaroline Morel
Howard Hughes Medical Institute, University of Massachusetts Chan Medical School
- SASaquib A. LakhaniCorresponding
Howard Hughes Medical Institute
- JKJason K. Kim
University of Massachusetts Chan Medical School
Topics & keywords
- Insulin resistance
- Inflammation
- Proinflammatory cytokine
- Adipose tissue
- Macrophage
- Adipose tissue macrophages
- Endocrinology
- Phenotype
- Good health and well-being