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非糖尿病和I型糖尿病患者轻度低血糖后葡萄糖处理受损。

Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans.

作者信息

Davis M R, Shamoon H

机构信息

Department of Medicine, Albert Einstein College of Medicine, New York, NY 10461.

出版信息

Metabolism. 1992 Feb;41(2):216-23. doi: 10.1016/0026-0495(92)90156-5.

DOI:10.1016/0026-0495(92)90156-5
PMID:1736045
Abstract

Insulin-mediated glucose disposal was studied immediately prior to and following moderate hypoglycemia in nondiabetic subjects and subjects with insulin-dependent (type I) diabetes mellitus (IDDM), the latter having varying epinephrine secretory capacities. Plasma insulin concentration was fixed throughout the study at approximately 300 to 400 pmol/L to avoid effects of waning insulin action and plasma glucose was clamped at either 5 mmol/L (euglycemic control) or at 3.1 mmol/L (hypoglycemic) periods of 120 minutes. Baseline (clamp 1) and postexperiment (clamp 2) periods were assessed for net glucose disposal (as a function of the exogenous glucose infusion rate) and glucose kinetics using 3H-glucose. In normal subjects, glucose disposal increased progressively by 132% during control studies but only by 57% with intervening hypoglycemia (P less than .005). Similarly, 33% during hypoglycemia, P less than .025). These changes were mediated by reduction of whole-body glucose uptake (rate of glucose disappearance [Rd], [3H]-3-glucose) and metabolic clearance rates with comparable suppression of hepatic glucose production in both groups. The increase in plasma free-fatty acids (FFA) following hypoglycemia was modest but greater in subjects with IDDM (P less than .01), whereas IDDM had reduced concentrations of epinephrine (P less than .01) and glucagon (P less than .005) during hypoglycemia. In subjects with IDDM but not in normal subjects, the change in posthypoglycemia glucose disposal was inversely correlated with the increase in plasma norepinephrine (R2 = .54, P less than .004) and epinephrine (R2 = .32, P less than .04). Glucose disposal did not correlate with other counterregulatory hormones, plasma FFA, or antecedent glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在非糖尿病受试者以及胰岛素依赖型(I型)糖尿病(IDDM)受试者(后者具有不同的肾上腺素分泌能力)中,在中度低血糖之前和之后立即研究胰岛素介导的葡萄糖处置情况。在整个研究过程中,血浆胰岛素浓度固定在约300至400 pmol/L,以避免胰岛素作用减弱的影响,并且将血浆葡萄糖在120分钟的时间段内钳制在5 mmol/L(正常血糖对照)或3.1 mmol/L(低血糖)。使用3H-葡萄糖评估基线期(钳夹1)和实验后期(钳夹2)的净葡萄糖处置(作为外源性葡萄糖输注速率的函数)和葡萄糖动力学。在正常受试者中,在对照研究期间葡萄糖处置逐渐增加了132%,但在中间有低血糖时仅增加了57%(P<0.005)。同样,低血糖期间为33%,P<0.025)。这些变化是由全身葡萄糖摄取减少(葡萄糖消失速率[Rd],[3H]-3-葡萄糖)和代谢清除率介导的,两组肝脏葡萄糖生成均受到类似抑制。低血糖后血浆游离脂肪酸(FFA)的增加幅度较小,但在IDDM受试者中更大(P<0.01),而IDDM在低血糖期间肾上腺素(P<0.01)和胰高血糖素(P<0.005)浓度降低。在IDDM受试者而非正常受试者中,低血糖后葡萄糖处置的变化与血浆去甲肾上腺素的增加呈负相关(R2 = 0.54,P<0.004)和肾上腺素(R2 = 0.32,P<0.04)。葡萄糖处置与其他反调节激素、血浆FFA或先前的血糖控制无关。(摘要截断于250字)

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