老年人胰岛素抵抗与动脉粥样硬化的关系

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。

Relationship between insulin resistance and atherosclerosis in the aged

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 atherosclerotic vascular disease (ASVD) increased, the levels of triglyceride (TG), cholesterol (CH), low density lipoprotein-cholesterol (LDL-C), fasting plasma glucose (FPG), 2 hour plasma glucose (2 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 atherosclerotic parameters increased (P<0. 05-<0. 001). The multivariate regression analysis showed that TG, CH, HDL-C, LDL-C levels and Ln (HOMA-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 atherosclerosis.