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乙醇对老年人碳水化合物代谢的影响。

Effects of ethanol on carbohydrate metabolism in the elderly.

作者信息

Boden G, Chen X, Desantis R, White J, Mozzoli M

机构信息

Division of Endocrinology/Metabolism, Temple University School of Medicine, Philadelphia, PA.

出版信息

Diabetes. 1993 Jan;42(1):28-34.

PMID:8420819
Abstract

We have previously reported that in young men, ethanol caused acute insulin resistance, but compensatory insulin secretion prevented deterioration of glucose tolerance (1). In this study, we tested the hypothesis that elderly men, because of their pre-existing insulin resistance and compromised insulin secretory capacity, may experience worsening of their glucose tolerance after ethanol. Nine elderly men (65.7 +/- 0.8 yr, BMI 25.8 +/- 1.4 kg/m2) received ethanol (13 mmol/kg for 30 min i.v.) or saline followed 30 min later by i.v. glucose (2.8 mmol/kg for 5 min). To determine the mechanism of the ethanol effect, six of the men underwent euglycemic-hyperinsulinemic (approximately 350 pM) clamping with simultaneous infusion of ethanol or saline. Muscle biopsies were obtained before and 1 and 4 h after insulin infusion. In all nine men, glucose concentrations after i.v. glucose were higher after ethanol than after saline, whereas insulin was the same and glucose tolerance decreased by 23% (Kg 2.41 +/- 0.2 vs. 1.86 +/- 0.1%/min, P < 0.01). Ethanol reduced insulin-stimulated glucose uptake from 40.6 +/- 3.1 to 25.6 +/- 1.9 mumol.kg-1.min-1 (-37%, P < 0.05), glucose oxidation from 11.7 +/- 1.1 to 7.0 +/- 0.7 mumol.kg-1.min-1 (-33%, P < 0.01), and glucose storage from 28.7 +/- 2.4 to 18.6 +/- 1.7 mumol.kg-1.min-1 (-35%, P < 0.01). Ethanol increased muscle lactate concentration from 0.49 +/- 0.14 to 1.99 +/- 0.99 mumol/mg protein (P < 0.05), but had no effects on muscle concentration of free glucose, G-6-P, and citrate concentrations, nor did it affect muscle GS activity.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们之前报道过,在年轻男性中,乙醇会引起急性胰岛素抵抗,但代偿性胰岛素分泌可防止糖耐量恶化(1)。在本研究中,我们检验了这样一个假设:老年男性由于其已存在的胰岛素抵抗和受损的胰岛素分泌能力,在摄入乙醇后可能会出现糖耐量恶化。九名老年男性(65.7±0.8岁,体重指数25.8±1.4kg/m2)接受静脉注射乙醇(13mmol/kg,持续30分钟)或生理盐水,30分钟后再静脉注射葡萄糖(2.8mmol/kg,持续5分钟)。为了确定乙醇作用的机制,其中六名男性在静脉输注乙醇或生理盐水的同时进行了正常血糖-高胰岛素血症(约350pM)钳夹试验。在胰岛素输注前以及输注后1小时和4小时采集肌肉活检样本。在所有九名男性中,静脉注射葡萄糖后的血糖浓度在乙醇处理后高于生理盐水处理后,而胰岛素水平相同,糖耐量下降了23%(K值从2.41±0.2降至1.86±0.1%/分钟,P<0.01)。乙醇使胰岛素刺激的葡萄糖摄取从40.6±3.1降至25.6±1.9μmol·kg-1·min-1(-37%,P<0.05),葡萄糖氧化从11.7±1.1降至7.0±0.7μmol·kg-1·min-1(-33%,P<0.01),葡萄糖储存从28.7±2.4降至18.6±1.7μmol·kg-1·min-1(-35%,P<0.01)。乙醇使肌肉乳酸浓度从0.49±0.14升至1.99±0.99μmol/mg蛋白质(P<0.05),但对肌肉中游离葡萄糖、6-磷酸葡萄糖和柠檬酸的浓度没有影响,也不影响肌肉糖原合酶活性。(摘要截断于250字)

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