期刊
CARDIOVASCULAR RESEARCH
卷 89, 期 3, 页码 604-613出版社
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvq360
关键词
CD36; Obesity; Insulin resistance; Macrophages; Adipocytes
资金
- NIH [P01 HL087018, P01 HL46403, HL072942]
- AHA Great Rivers Affiliate [0825685D]
- Lerner Research Institute
- Cleveland Clinic
Aims Obesity and hyperlipidaemia are associated with insulin resistance (IR); however, the mechanisms responsible remain incompletely understood. Pro-atherogenic hyperlipidaemic states are characterized by inflammation, oxidant stress, and pathophysiologic oxidized lipids, including ligands for the scavenger receptor CD36. Here we tested the hypothesis that the absence of CD36 protects mice from IR associated with diet-induced obesity and hyperlipidaemia. Methods and results Adipose tissue from CD36(-/-) mice demonstrated a less inflammatory phenotype and improved insulin signalling in vivo and at the level of the adipocyte and macrophage. The pathophysiologic ligand oxidized low-density lipoprotein (oxLDL) activated c-Jun N-terminal kinase (JNK) and disrupted insulin signalling in both adipocytes and macrophages in a CD36-dependent manner. Macrophages isolated from CD36(-/-) mice after high-fat diet feeding elicited less JNK activation and inhibition of insulin signalling in adipocytes after co-culture compared with wild-type macrophages. Conclusion These data suggest that a CD36-dependent inflammatory paracrine loop between adipocytes and macrophages facilitates chronic inflammation and contributes to IR common in obesity and dyslipidaemia.
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