Shelmet J J, Reichard G A, Skutches C L, Hoeldtke R D, Owen O E, Boden G
Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.
J Clin Invest. 1988 Apr;81(4):1137-45. doi: 10.1172/JCI113428.
To study the mechanism of the diabetogenic action of ethanol, ethanol (0.75 g/kg over 30 min) and then glucose (0.5 g/kg over 5 min) were infused intravenously into six normal males. During the 4-h study, 21.8 +/- 2.1 g of ethanol was metabolized and oxidized to CO2 and H2O. Ethanol decreased total body fat oxidation by 79% and protein oxidation by 39%, and almost completely abolished the 249% rise in carbohydrate (CHO) oxidation seen in controls after glucose infusion. Ethanol decreased the basal rate of glucose appearance (GRa) by 30% and the basal rate of glucose disappearance (GRd) by 38%, potentiated glucose-stimulated insulin release by 54%, and had no effect on glucose tolerance. In hyperinsulinemic-euglycemic clamp studies, ethanol caused a 36% decrease in glucose disposal. We conclude that ethanol was a preferred fuel preventing fat, and to lesser degrees, CHO and protein, from being oxidized. It also caused acute insulin resistance which was compensated for by hypersecretion of insulin.
为研究乙醇致糖尿病作用的机制，将乙醇（0.75克/千克，持续30分钟）然后葡萄糖（0.5克/千克，持续5分钟）静脉输注到6名正常男性体内。在4小时的研究期间，21.8±2.1克乙醇被代谢并氧化为二氧化碳和水。乙醇使全身脂肪氧化减少79%，蛋白质氧化减少39%，并几乎完全消除了对照组在输注葡萄糖后出现的249%的碳水化合物（CHO）氧化增加。乙醇使基础葡萄糖出现率（GRa）降低30%，基础葡萄糖消失率（GRd）降低38%，使葡萄糖刺激的胰岛素释放增强54%，且对葡萄糖耐量无影响。在高胰岛素-正常血糖钳夹研究中，乙醇使葡萄糖处置减少36%。我们得出结论，乙醇是一种优先燃料，可防止脂肪以及程度较轻的CHO和蛋白质被氧化。它还引起急性胰岛素抵抗，胰岛素分泌增多可对此进行代偿。
