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

Myoung Sook Han, Dae Young Jung, Caroline Morel, Saquib A. Lakhani, Jason K. Kim, Richard A. Flavell, and Roger J. Davis

The cJun NH2-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 proinflammatory macrophage polarization. These studies demonstrate that JNK in macrophages is required for the establishment of obesity-induced insulin resistance and inflammation.

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