Service d'Endocrinologie, Diabétologie et Maladies Métaboliques, Hôpital du Bocage, CHU Dijon, France.
Fundam Clin Pharmacol. 2009 Dec;23(6):681-5. doi: 10.1111/j.1472-8206.2009.00739.x. Epub 2009 Jul 24.
Patients with type 2 diabetes feature important modification of both low density lipoprotein (LDL) and high density lipoprotein particles which are likely to play an important role in the development of atherosclerosis. Although plasma LDL cholesterol level is usually normal in type 2 diabetic patients, LDLs show a significant increase in their plasma residence time which may promote cholesterol deposition in the arterial wall. Moreover, important qualitative abnormalities of LDLs, potentially atherogenic, are observed in type 2 diabetic patients: small dense, triglyceride-rich, LDL particles (known as subclass B), oxidized LDL and glycated LDL. All these qualitative modification of LDLs amplify the atherosclerotic process. Plasma high density lipoprotein (HDL) cholesterol is decreased in type 2 diabetes related to increased catabolism of HDL particles. One of the mechanism responsible for increased catabolism of HDLs is hypertriglyceridemia, promoting through cholesteryl ester transfer protein (CETP) the transfer of triglycerides (TG) to HDL leading to the formation of TG-rich HDLs which are very good substrates for hepatic lipase, enzyme in charge of HDLs catabolism. The reduction in plasma adiponectin level, observed in type 2 diabetes may be another mechanism involved in the diminution of HDL cholesterol. Furthermore, qualitative abnormalities of HDLs are described in type 2 diabetes: enrichment in triglycerides and glycation, which may impair HDL-mediated cholesterol efflux and reverse cholesterol transport. In addition to their role in reverse cholesterol transport, HDLs usually show antioxidative, anti-inflammatory, anti-thrombotic and endothelium-dependent vasorelaxant effects. It has been shown that HDLs from patients with type 2 diabetes have a significant reduction in their antioxidative and endothelium-dependent vasorelaxant properties.
2 型糖尿病患者的低密度脂蛋白（LDL）和高密度脂蛋白颗粒均发生重要修饰，这可能在动脉粥样硬化的发生中发挥重要作用。虽然 2 型糖尿病患者的血浆 LDL 胆固醇水平通常正常，但 LDL 在血浆中的停留时间显著增加，这可能促进胆固醇在动脉壁中的沉积。此外，2 型糖尿病患者 LDL 存在重要的、潜在致动脉粥样硬化的质量异常：小而密、富含甘油三酯的 LDL 颗粒（称为 B 亚类）、氧化 LDL 和糖化 LDL。所有这些 LDL 的质量修饰均放大了动脉粥样硬化过程。2 型糖尿病患者的血浆高密度脂蛋白（HDL）胆固醇降低与 HDL 颗粒的分解代谢增加有关。导致 HDL 分解代谢增加的机制之一是高甘油三酯血症，通过胆固醇酯转移蛋白（CETP）促进甘油三酯（TG）向 HDL 的转移，导致富含 TG 的 HDL 形成，而富含 TG 的 HDL 是肝脂肪酶分解代谢的极好底物，肝脂肪酶是负责 HDL 分解代谢的酶。在 2 型糖尿病中观察到的血浆脂联素水平降低可能是 HDL 胆固醇减少的另一个机制。此外，在 2 型糖尿病中描述了 HDL 的质量异常：甘油三酯和糖化增加，这可能损害 HDL 介导的胆固醇流出和胆固醇逆向转运。除了在胆固醇逆向转运中的作用外，HDL 通常具有抗氧化、抗炎、抗血栓和内皮依赖性血管舒张作用。已经表明，2 型糖尿病患者的 HDL 抗氧化和内皮依赖性血管舒张特性显著降低。
