Ethanol causes acute inhibition of carbohydrate, fat, and protein oxidation and insulin resistance.
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.
Shelmet
J J
JJ
Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania 19140.
Reichard
G A
GA
Skutches
C L
CL
Hoeldtke
R D
RD
Owen
O E
OE
Boden
G
G
D000085:Acetates / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002151:Calorimetry; D050260:Carbohydrate Metabolism; D000431:Ethanol / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism*; D011972:Receptor, Insulin / Q000378:metabolism
D000085:Acetates; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D011506:Proteins; D000431:Ethanol; D011972:Receptor, Insulin