Pastromas Socrates, Terzi Angela-Beth, Tousoulis Dimitris, Koulouris Spyridon
First Department of Cardiology, Evagelismos General Hospital of Athens, Greece.
Int J Cardiol. 2008 May 7;126(1):3-12. doi: 10.1016/j.ijcard.2007.04.172. Epub 2007 Aug 8.
Atherosclerotic disease is the leading cause of both morbidity and mortality in patients with type 2 diabetes. In these patients, postprandial dyslipidemia include not only quantitative but also qualitative abnormalities of lipoproteins which are potentially atherogenic and seems to be a significant risk factor for cardiovascular disease since there is evidence that it results in endothelial dysfunction and enhanced oxidative stress. The most common pattern of postprandial dyslipidemia in diabetes consists of high concentrations of triglycerides, higher VLDLs production by the liver and a decrease in their clearance, a predominance of small dense LDL particles, and reduced levels of HDL. The cause of this postprandial dyslipidemia in diabetes is complex and involves a variety of factors including hyperinsulinemia, insulin resistance, hyperglycemia and disturbed fatty acid metabolism. Numerous clinical studies have shown that postprandial dyslipidemia is associated with endothelial dysfunction in type 2 diabetes and with alterations in other surrogate markers in the cascade of atherosclerosis. Current published guidelines indicate that in diabetics the primary lipid target is LDL<100 mg/dL (70 mg/dL in very high-risk patients) and the most appropriate class of drugs are statins although the issue of postprandial dyslipidemia has not been specifically addressed so far. Moreover, several other classes of medications (fibrates, niacin and antidiabetic drugs) as well as non-pharmacological interventions (i.e. diet, smoking cessation and exercise) can be used to treat lipid and lipoprotein abnormalities associated with insulin resistance and type 2 diabetes. These type of interventions may be more appropriate to ameliorate postprandial dyslipidemia. However, this remains to be confirmed on clinical grounds.
动脉粥样硬化疾病是2型糖尿病患者发病和死亡的主要原因。在这些患者中，餐后血脂异常不仅包括脂蛋白数量上的异常，还包括质量上的异常，这些异常具有潜在的致动脉粥样硬化性，并且似乎是心血管疾病的一个重要危险因素，因为有证据表明它会导致内皮功能障碍和氧化应激增强。糖尿病患者餐后血脂异常最常见的模式包括甘油三酯浓度升高、肝脏产生的极低密度脂蛋白（VLDL）增加及其清除减少、小而密低密度脂蛋白颗粒占主导以及高密度脂蛋白（HDL）水平降低。糖尿病患者餐后血脂异常的原因很复杂，涉及多种因素，包括高胰岛素血症、胰岛素抵抗、高血糖和脂肪酸代谢紊乱。大量临床研究表明，餐后血脂异常与2型糖尿病患者的内皮功能障碍以及动脉粥样硬化级联反应中其他替代标志物的改变有关。目前已发表的指南指出，糖尿病患者的主要血脂目标是低密度脂蛋白（LDL）<100 mg/dL（极高危患者为70 mg/dL），最合适的药物类别是他汀类药物，尽管餐后血脂异常问题迄今尚未得到专门解决。此外，其他几类药物（贝特类、烟酸类和抗糖尿病药物）以及非药物干预措施（如饮食、戒烟和运动）可用于治疗与胰岛素抵抗和2型糖尿病相关的脂质和脂蛋白异常。这类干预措施可能更适合改善餐后血脂异常。然而，这仍有待临床证实。
