Pathogenic role of scavenger receptor CD36 in the metabolic syndrome and diabetes.

Overview

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.