title: Pathogenic role of scavenger receptor CD36 in the metabolic syndrome and diabetes.
abstract: Obesity is increasing at epidemic proportions in the United States and is a major contributor to the development of both metabolic syndrome (glucose intolerance, dyslipidemia, hypertension) and atherosclerotic cardiovascular disease. A wide body of evidence has linked systemic low-grade inflammation as underlying obesity and insulin-resistant states via monocyte/macrophage activation. Transgenic deletion of scavenger receptor type B CD36 in rodents has suggested a pivotal role for CD36 in mediating inflammation, insulin resistance, and atherogenesis through transport of fatty acids and uptake of oxidized lipids, respectively. CD36 signaling pathways involving c-Jun N-terminal kinase (JNK) activation and Toll-like receptors have been implicated in the induction of insulin resistance. This review will focus on the pathogenic role of CD36 receptors in metabolic syndrome and type 2 diabetes.
authors.affiliation: Department of Cell Biology, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic Foundation, Ohio 44195, USA.
authors.forename: David J
authors.initials: DJ
authors.lastname: Kennedy
authors.forename: Sangeeta R
authors.initials: SR
authors.lastname: Kashyap
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D050197:Atherosclerosis; D018955:CD36 Antigens / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000209:etiology* / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D007333:Insulin Resistance; D008264:Macrophages / Q000378:metabolism; D024821:Metabolic Syndrome / Q000209:etiology* / Q000378:metabolism*; D008954:Models, Biological; D015398:Signal Transduction
chemical_list: D018955:CD36 Antigens