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目的探讨初诊伴微量白蛋白尿(MU)的2型糖尿病患者内皮功能障碍与胰岛功能改变的关系。方法选择符合1999年WHO糖尿病诊断标准且尿白蛋白排泄率(UAER)≥20μg/min、<200μg/min,除外其他MU的原因且空腹血糖(FBS)>10 mmol/L与餐后2小时血糖(2 hBS)>15 mmol/L的初诊2型糖尿病患者32例,观察体质量指数(BMI)、腰臀比(WHR)、FBS、空腹胰岛素(FINS)、空腹C肽(FCP)、果糖胺(FA)、UAER、尿内皮素(UET-1)、血内皮素(SET-1),计算稳态模型(HOMA)模型β细胞功能指数(HOMA-Is),对应用胰岛素强化治疗前与血糖下降(避免低血糖反应且FBS<7 mmol/L与2 hBS<9 mmol/L)平稳2周后上述指标进行对比。结果治疗前后FBS(15.01±3.15)mmol/L vs(6.81±0.86)mmol/L,FA(3.90±0.38)mmol/L vs(2.41±0.29)mmol/L,HOMA-Is(2.79±0.89 vs 4.32±0.5),UAER(53.07±19.83)μg/min vs(21.65±8.16)μg/min,UET-1(244.56±19.30)pg/min vs(142.12±27.95)pg/min,SET-1(153.34±31.52)ng/L vs(103.55±20.77)ng/L,相互比较差异有统计学意义(P<0.01),FBS、HOMA-Is分别与UAER、UET-1、SET-1有显著的偏相关性(P<0.01或<0.05)。结论肾内皮功能障碍及MU的出现与糖尿病患者胰岛功能缺陷后胰岛素缺乏并且由此继发的高血糖有关,胰岛功能缺陷在糖尿病肾病的发生发展中不容忽视。
Objective To investigate the relationship between endothelial dysfunction and pancreatic islet function in newly diagnosed type 2 diabetic patients with microalbuminuria (MU). Methods According to the WHO diagnostic criteria of WHO in 1999, the urinary albumin excretion rate (UAER) ≥20μg / min, except 200μg / min except MU, the fasting blood glucose (FBS)> 10mmol / 32 patients with newly diagnosed type 2 diabetes mellitus (2 hBS)> 15 mmol / L were enrolled in this study. The body mass index (BMI), WHR, FBS, fasting insulin (FINS), fasting C-peptide (FA), UAER, UET-1 and SET-1, and calculated HOMA-Isometabolic Index (HOMA-Is) Decreased (to avoid hypoglycemic response and FBS <7 mmol / L and 2 hBS <9 mmol / L) were stable for 2 weeks after the above indicators were compared. Results FBS (15.01 ± 3.15) mmol / L vs (6.81 ± 0.86) mmol / L, FA (3.90 ± 0.38) mmol / L vs (2.41 ± 0.29) mmol / L and HOMA-Is ± 0.5, UAER 53.07 ± 19.83 μg / min vs 21.65 ± 8.16 μg / min, UET-1 244.56 ± 19.30 pg / min vs 142.12 ± 27.95 pg / 31.52) ng / L vs 103.55 ± 20.77 ng / L, respectively (P <0.01). There was a significant correlation between FBS and HOMA-Is with UAER, UET-1 and SET- (P <0.01 or <0.05). Conclusions Renal endothelium dysfunction and the occurrence of MU are associated with insulin deficiency and subsequent hyperglycemia in diabetic patients. The islet dysfunction can not be ignored in the development of diabetic nephropathy.