老年人胰岛素抵抗与动脉粥样硬化的关系

Relationship between insulin resistance and atherosclerosis in the aged

目的:探讨胰岛素抵抗(IR)与动脉粥样硬化(AS)的关系。方法:在60岁以上的人群中筛查,体检,记录病史,进行口服75g葡萄糖耐量试验(75 g OGTT)。抽血检查血脂及胰岛素水平,B型超声检查双侧颈总动脉内中膜厚度(IMT)。采用稳态模型(HOMA Model)计算胰岛素抵抗指数(HOMA-IR),根据HOMA-IR值182例研究对象被分为4组,比较各组的危险因素及颈动脉粥样硬化指标。结果:随着HOMA-IR值升高,高血糖(糖耐量低减及糖尿病)、高血压(HPT)、动脉粥样硬化性血管疾病(ASVD)发病率增高(P<0．05～<0．001),甘油三酯 (TG)、胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、空腹血糖(FPG)、服糖后2 h血糖(2 h PG)、空腹胰岛素 (FINS)水平增高(P<0．05-<0．001),高密度脂蛋白胆固醇(HDL-C)水平降低(P<0．05),各项AS指标升高 (P<0．01-<0．001)。多元回归分析结果显示,TG、TC、HDL-C、LDL-C、Ln(HOMA-IR)与IMT独立相关 (P<0.05-<0．001),是IMT增高的危险因素。结论:胰岛素抵抗参与动脉粥样硬化的形成。

Objective： To investigate the relationship between insulin resistance （IR） and atherosclerosis （AS） in the aged. Methods ： The subjects were recruited among those who were over 60 years. All participants underwent physical examination, medical history taking and 75 g oral glucose tolerance test. Venous blood was sampled for the measurement of serum concentrations of lipid and insulin. The intima-media thickness （IMT） was observed in bilateral common carotid arteries by B-mode ultrasound. （Insulin resistance index was calculated by homeostasis model assessment （HOMA-IR）. Subjects were stratified in quartiles according to HOMA-IR. Risk factors and atherosclerotic parameters were compared. Results： With the increasing of HOMA-IR, the incidence of hyperglycemia （IGT and DM）, hypertension （HPT） and atheroschrotic vascular disease （ASVD） increased, the levels of triglycerlde （TG）, cholesterol （CH）, low density lipoprotein-cholesterol （LDL-C）, fasting plasma glucose （FPG）, 2 hour plasma glucose 42 h PG） and fasting insulin （FINS） increased （P〈0. 05-〈0. 001 all）, the level of high density lipoprotein-cholesterol （HDL-C） decreased （P〈0.05）. All the atherosclerotie parameters increased （P〈0.05-〈0. 001）. The multivariate regression analysis showed that TG, CH, HDL-C, LDL-C levels and Ln （FIOMA-IR） were related to IMT （P〈 0. 05-〈0. 001）. They were the risk factors for the increasing of IMT. Conclusion： Insulin resistance is implicated in the pathogenesis of atheroselerosis.