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目的:为了探讨糖尿病高血糖状态对胰岛功能、肾脏血管内皮毒性作用与胰岛素抵抗的临床意义。方法:选择符合1999年WHO糖尿病诊断标准且伴微量白蛋白尿(MU)的新诊2型糖尿病患者32例,观察体重指数(BMI)、腰臀比(WHR)、空腹血糖(FBS)、空腹胰岛素(FINS)、空腹C肽(FCP)、果糖胺(FA)、尿白蛋白排泄率(UAER)、尿内皮素(UET-1)、血内皮素(SET-1),计算稳态模型β细胞功能指数(HOMA-Is)与胰岛素抵抗指数(HOMA-IR),应用胰岛素强化治疗,血糖下降平稳2周后复查上述指标进行对比。结果:治疗前后FBS[(15.01±3.15)mmol/Lvs(6.81±0.86)mmol/L]、FA[(3.90±0.38)mmol/Lvs(2.41±0.29)mmol/L]、UAER[(53.07±19.83)μg/minvs(21.65±8.16)μg/min]、UET-1[(244.56±19.30)pg/minvs(142.12±27.95)pg/min]、SET-1[(153.34±31.52)ng/Lvs(103.55±20.77)ng/L]比较,差异有统计学意义(P<0.01),FBS、HOMA-Is、HOMA-IR分别与UAER、UET-1、SET-1有相关关系(P<0.01或<0.05)。结论:糖尿病肾病的发生发展与胰岛素抵抗、持续性高血糖毒性损害及胰岛功能减退而失去正常效应胰岛素水平对肾脏血管内皮的保护作用有关;胰岛素抵抗、胰岛功能减退、高血糖与内皮功能障碍的相互作用可能是关键环节。
Objective: To investigate the clinical significance of diabetic hyperglycemia on islet function, renal vascular endothelium toxicity and insulin resistance. Methods: Thirty-two newly diagnosed type 2 diabetic patients with diagnostic criteria of WHO in 1999 and with microalbuminuria (MU) were selected. Body mass index (BMI), WHR, fasting blood glucose (FBS) FINS, FCP, FA, UAER, UET-1 and SET-1 were calculated, and the steady-state model β Cell function index (HOMA-Is) and insulin resistance index (HOMA-IR), the application of insulin-intensive therapy, blood glucose decreased after 2 weeks of stable review of the above indicators for comparison. Results: Before and after treatment, the levels of FBS in serum were significantly higher in FBS group than those in control group (F (15.01 ± 3.15) mmol / L vs 6.83 ± 0.86 mmol / L, FA [3.90 ± 0.38 mmol / L vs 2.41 ± 0.29 mmol / L] ), SET-1 [(153.34 ± 31.52) ng / Lvs (103.55 ± 8.16) μg / min], UET-1 [(244.56 ± 19.30) pg / min vs (142.12 ± 27.95) pg / ± 20.77 ng / L], the difference was statistically significant (P <0.01). There was a significant correlation between FBS, HOMA-Is and HOMA-IR and UAER, UET-1 and SET- ). Conclusion: The occurrence and development of diabetic nephropathy is related to the protective effect of insulin resistance, persistent hyperglycemic toxicity and loss of islet function, and loss of normal effect insulin on renal vascular endothelium. Insulin resistance, islet dysfunction, hyperglycemia and endothelial dysfunction Interaction may be the key link.