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在无并发症的1型糖尿病中,胰岛素诱导的大动脉僵硬度降低受损。

Insulin-induced decrease in large artery stiffness is impaired in uncomplicated type 1 diabetes mellitus.

作者信息

Westerbacka J, Uosukainen A, Mäkimattila S, Schlenzka A, Yki-Järvinen H

机构信息

Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland.

出版信息

Hypertension. 2000 May;35(5):1043-8. doi: 10.1161/01.hyp.35.5.1043.

Abstract

Normal insulin action in vivo involves a decrease in stiffness of large arteries (a decrease in aortic pressure augmentation). We determined whether the ability of insulin to decrease arterial stiffness is altered in uncomplicated type 1 diabetes. Nine type 1 diabetic men (age 28+/-2 years, body mass index 24+/-1 kg/m(2)) and 9 matched normal men were studied under normoglycemic hyperinsulinemic (sequential 2-hour insulin infusions of 1 [step 1] and 2 [step 2] mU x kg(-1) x min(-1)) conditions. Central aortic pressure waveforms were synthesized from those recorded in periphery with applanation tonometry on the radial artery and a validated reverse transfer function to construct the central aortic pressure wave every 30 minutes. This allowed the determination of aortic augmentation (the pressure difference between the first and the second systolic peaks) and the augmentation index (augmentation divided by pulse pressure), as the measure of stiffness of large arteries. Whole-body glucose uptake was 44% (step 1) and 37% (step 2) lower (P<0.001) in the diabetic patients than in the normal subjects. At baseline, before the insulin infusion, augmentation averaged 0+/-1 and 2+/-1 mm Hg (NS) and the augmentation index was -1.5+/-4.5% and 4.0+/-3.7% (NS) in the normal and diabetic subjects, respectively. After 1 hour of hyperinsulinemia, the augmentation index had decreased significantly (P<0.01) to -9.5+/-4.8% in the normal subjects but remained at 4.4+/-4.2% in the diabetic patients. A significant decrease was not observed in the diabetic patients until 150 minutes (-1.2+/-4.1%, P<0.05 versus baseline). Whole-body glucose uptake was significantly inversely correlated with the change in the augmentation index during step 1 (r=-0.61, P<0.01). Insulin resistance in type 1 diabetes involves a defect in the ability of insulin to decrease central aortic pressure. This defect could predispose these patients to premature stiffening of large arteries.

摘要

胰岛素在体内的正常作用包括大动脉僵硬度降低(主动脉压力增强减弱)。我们确定了在无并发症的1型糖尿病患者中,胰岛素降低动脉僵硬度的能力是否发生改变。对9名1型糖尿病男性患者(年龄28±2岁,体重指数24±1kg/m²)和9名匹配的正常男性在正常血糖高胰岛素血症(连续2小时输注胰岛素,剂量分别为1[步骤1]和2[步骤2]mU·kg⁻¹·min⁻¹)条件下进行研究。通过在桡动脉上应用压平式眼压计记录外周压力波形,并使用经过验证的反向传递函数,每30分钟构建一次中心主动脉压力波,从而合成中心主动脉压力波形。这使得能够确定主动脉增强(第一个和第二个收缩峰之间的压力差)和增强指数(增强值除以脉压),作为大动脉僵硬度的指标。糖尿病患者的全身葡萄糖摄取在步骤1时比正常受试者低44%,在步骤2时低37%(P<0.001)。在胰岛素输注前的基线时,正常受试者和糖尿病受试者的增强平均值分别为0±1和2±1mmHg(无显著性差异),增强指数分别为-1.5±4.5%和4.0±3.7%(无显著性差异)。高胰岛素血症1小时后,正常受试者的增强指数显著降低(P<0.01)至-9.5±4.8%,而糖尿病患者的增强指数仍保持在4.4±4.2%。直到150分钟时,糖尿病患者的增强指数才出现显著下降(-1.2±4.1%,与基线相比P<0.05)。在步骤1期间,全身葡萄糖摄取与增强指数的变化显著负相关(r=-0.61,P<0.01)。1型糖尿病中的胰岛素抵抗涉及胰岛素降低中心主动脉压力能力的缺陷。这种缺陷可能使这些患者易患大动脉过早僵硬。

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