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

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetates / blood
  • Adult
  • Blood Glucose / metabolism
  • Calorimetry
  • Carbohydrate Metabolism*
  • Ethanol / pharmacology*
  • Fatty Acids, Nonesterified / blood
  • Humans
  • Insulin / metabolism
  • Insulin Resistance*
  • Lipid Metabolism*
  • Liver / metabolism
  • Male
  • Oxidation-Reduction
  • Proteins / metabolism*
  • Receptor, Insulin / metabolism


  • Acetates
  • Blood Glucose
  • Fatty Acids, Nonesterified
  • Insulin
  • Proteins
  • Ethanol
  • Receptor, Insulin