期刊
METABOLIC SYNDROME AND RELATED DISORDERS
卷 9, 期 4, 页码 239-245出版社
MARY ANN LIEBERT INC
DOI: 10.1089/met.2011.0003
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资金
- American Heart Association Great Rivers Affiliate [0825685D]
- Lerner Research Institute
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.
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