Ethanol causes acute inhibition of carbohydrate, fat, and protein oxidation and insulin

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 H20. 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 de-creased the basal rate of glucose appearance (GR.) by 30 % and the basal rate of glucose disappearance (GR,) by 38%, poten-tiated 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 dis-posal. We conclude that ethanol was a preferred fuel prevent-ing 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