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

See allHide authors and affiliations

Science  06 Dec 2012:
DOI: 10.1126/science.1227568

You are currently viewing the abstract.

View Full Text


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.

  • * Present Address: Department of Pediatrics, Sanford University School of Medicine, Sioux Falls, SD 57117, USA.

View Full Text