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目的研究2型糖尿病下肢血管病变患者与单纯2型糖尿病患者晚期糖基化终末产物(AGEs)水平。方法采用竞争性酶联免疫吸附试验法(ELISA)测定2型糖尿病伴下肢血管病变组(DM1,n=75),单纯2型糖尿病组(DM2,n=40),正常对照组(NC,n=35)的AGEs。结果AGEs在DM1组高于DM2组与NC组,且有统计学差异(P<0.05)。对糖尿病下肢血管病变危险因素进行Logis-tic回归分析结果显示:去除常数项后,年龄、病程、纤维蛋白原和AGEs四项是大血管病变的主要危险因素(P<0.05),OR值分别为1.065,1.043,1.324,2.012。结论糖尿病下肢血管病变时AGEs明显升高,说明蛋白非酶糖基化可能是糖尿病下肢血管病变发生的病理机制之一。控制糖尿病患者糖代谢紊乱可以降低蛋白非酶糖基化过程。
Objective To investigate the levels of advanced glycation end products (AGEs) in patients with type 2 diabetes mellitus and those with type 2 diabetes mellitus. Methods DM2 (n = 75), type 2 diabetes mellitus (DM2, n = 40) and normal control group (nc, n) were determined by competitive enzyme linked immunosorbent assay (ELISA) = 35) AGEs. Results AGEs were higher in DM1 group than in DM2 group and NC group (P <0.05). Logis-tic regression analysis of risk factors of lower extremity vascular disease in diabetic patients showed that age, duration of disease, fibrinogen and AGEs were the major risk factors for macrovascular disease after removing the constant term (P <0.05), and OR values were 1.065, 1.043, 1.324, 2.012. Conclusion The AGEs of diabetic lower extremity vascular lesions were significantly increased, indicating that non-enzymatic glycation of protein may be one of the pathological mechanisms of diabetic lower extremity vascular lesions. Control of diabetic patients with glucose metabolism disorder can reduce protein non-enzymatic glycosylation process.