Hsueh Willa A, Law Ronald
Division of Endocrinology, Diabetes, and Hypertension, University of California-Los Angeles School of Medicine, Los Angeles, California 90095-7073, USA.
Am J Cardiol. 2003 Aug 18;92(4A):3J-9J. doi: 10.1016/s0002-9149(03)00610-6.
Recent evidence suggests that progression of insulin resistance parallels progression of atherosclerosis. Fat plays an integral role in the development of type 2 diabetes and vascular injury. The balance of adipose-derived substances, including free fatty acids, tumor necrosis factor-alpha, leptin, adiponectin, and plasminogen activator inhibitor-1, determine both insulin action and the state of vascular inflammation. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands promote the balance of these substances to enhance insulin-mediated glucose uptake and decrease inflammation. PPAR-gamma ligands reverse the major defect of the insulin resistance syndrome and have important effects that inhibit atherosclerosis, improve endothelial cell function, and attenuate inflammation. Although more research is needed, data suggest that PPAR-gamma ligands may prevent the progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis.
近期证据表明，胰岛素抵抗的进展与动脉粥样硬化的进展平行。脂肪在2型糖尿病和血管损伤的发生发展中起着不可或缺的作用。包括游离脂肪酸、肿瘤坏死因子-α、瘦素、脂联素和纤溶酶原激活物抑制剂-1在内的脂肪源性物质的平衡，决定了胰岛素作用和血管炎症状态。过氧化物酶体增殖物激活受体-γ（PPAR-γ）配体促进这些物质的平衡，以增强胰岛素介导的葡萄糖摄取并减轻炎症。PPAR-γ配体可逆转胰岛素抵抗综合征的主要缺陷，并具有抑制动脉粥样硬化、改善内皮细胞功能和减轻炎症的重要作用。尽管还需要更多研究，但数据表明PPAR-γ配体可能预防胰岛素抵抗向糖尿病的进展以及内皮功能障碍向动脉粥样硬化的进展。
