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

J J Shelmet; G A Reichard; C L Skutches; R D Hoeldtke; O E Owen; G Boden

doi:10.1172/JCI113428

Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.

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Published in Volume 81, Issue 4 on April 1, 1988
J Clin Invest. 1988;81(4):1137–1145. https://doi.org/10.1172/JCI113428.
© 1988 The American Society for Clinical Investigation

Published April 1, 1988 - Version history

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.