Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
Diabetes Metab Res Rev. 2011 Jul;27(5):488-92. doi: 10.1002/dmrr.1188.
In addition to the important role of advanced glycation end products (AGEs) in the pathogenesis of diabetic vascular complications, recent data suggest that advanced glycation end products can also impair insulin action in vitro. We have investigated whether circulating advanced glycation end products are associated with insulin resistance in human subjects independent of metabolic parameters.
Two hundred and seven healthy non-obese non-diabetic subjects (97 male, 110 female) were recruited from the community. Serum levels of advanced glycation end products, adiponectin, malondialdehyde and high sensitivity C-reactive protein were assayed. Insulin resistance was determined by the homeostasis model assessment index (HOMA-IR).
Male subjects had significantly higher body mass index, waist circumference and lower adiponectin level than female subjects and were more insulin resistant. Serum advanced glycation end products (3.67 ± 1.15 unit/mL versus 3.23 ± 1.15, p < 0.05) and malondialdehyde levels (p < 0.05) were also higher in male than in female subjects. Serum advanced glycation end products correlated with HOMA-IR in both male (r = 0.32, p = 0.004) and female subjects (r = 0.28, p = 0.003). Serum adiponectin inversely correlated with HOMA-IR in female (r = - 0.38, p < 0.001) but not in male subjects. On multiple regression analysis, serum AGEs remained an independent determinant of HOMA-IR even after adjusting for age, gender, body mass index, waist, smoking, adiponectin and markers of oxidative stress and inflammation.
Formation and accumulation of advanced glycation end products progress during normal ageing. We have demonstrated that the circulating level of advanced glycation end products is associated with insulin resistance even in non-obese, non-diabetic subjects independent of adiponectin.
除了晚期糖基化终产物(AGEs)在糖尿病血管并发症发病机制中的重要作用外,最近的数据还表明,晚期糖基化终产物也可以体外损害胰岛素作用。我们研究了循环晚期糖基化终产物是否与人体胰岛素抵抗有关,而不考虑代谢参数。
从社区招募了 207 名健康的非肥胖非糖尿病受试者(97 名男性,110 名女性)。测定血清晚期糖基化终产物、脂联素、丙二醛和高敏 C 反应蛋白水平。用稳态模型评估指数(HOMA-IR)测定胰岛素抵抗。
男性受试者的体重指数、腰围明显高于女性,脂联素水平较低,胰岛素抵抗也较高。男性血清晚期糖基化终产物(3.67±1.15 单位/ml 与 3.23±1.15,p<0.05)和丙二醛水平也高于女性。男性和女性血清晚期糖基化终产物与 HOMA-IR 均相关(男性 r=0.32,p=0.004;女性 r=0.28,p=0.003)。血清脂联素与女性 HOMA-IR 呈负相关(r=-0.38,p<0.001),但与男性无关。多元回归分析显示,即使在调整了年龄、性别、体重指数、腰围、吸烟、脂联素以及氧化应激和炎症标志物后,血清 AGEs 仍然是 HOMA-IR 的独立决定因素。
晚期糖基化终产物的形成和积累在正常衰老过程中不断进展。我们已经证明,即使在非肥胖、非糖尿病患者中,循环晚期糖基化终产物水平与胰岛素抵抗有关,而与脂联素无关。