THE INHIBITION OF GLUCONEOGENESIS FOLLOWING ALCOHOL IN HUMANS

Accurate quantification of gluconeogenic flux following alcohol ingest ion in overnight-fasted humans has yet to be reported. [2-C-13(1)]glyc erol, [U-C-13(6)]glucose, [1-H-2(1)]galactose, and acetaminophen were infused in normal men before and after the consumption of 48 g alcohol or a placebo to quantify gluconeogenesis, glycogenolysis, hepatic glu cose production, and intrahepatic gluconeogenic precursor availability . Gluconeogenesis decreased 45% vs, the placebo (0.56 +/- 0.05 to 0.44 +/- 0.04 mg . kg(-1). min(-1) vs. 0.44 +/- 0.05 to 0.63 +/- 0.09 mg k g-l min-l, respectively, P < 0.05) in the 5 h after alcohol ingestion, and total gluconeogenic flux was lower after alcohol compared with pl acebo. Glycogenolysis fell over time after both the alcohol and placeb o cocktails, from 1.46-1.47 mg kg-l min-l to 1.35 +/- 0.17 mg . kg(-1) . min(-1) (alcohol) and 1.26 +/- 0.20 mg . kg(-1). min(-1), respective ly (placebo, P < 0.05 vs. baseline). Hepatic glucose output decreased 12% after alcohol consumption, from 2.03 +/- 0.21 to 1.79 +/- 0.21 mg . kg(-1). min(-1) (P < 0.05 vs. baseline), but did not change followin g the placebo. Estimated intrahepatic gluconeogenic precursor availabi lity decreased 61% following alcohol consumption (P < 0.05 vs. baselin e) but was unchanged after the placebo (P < 0.05 between treatments). We conclude from these results that gluconeogenesis is inhibited after alcohol consumption in overnight-fasted men, with a somewhat larger d ecrease in availability of gluconeogenic precursors but a smaller effe ct on glucose production and no effect on plasma glucose concentration s. Thus inhibition of flux into the gluconeogenic precursor pool is co mpensated by changes in glycogenolysis, the fate of triose-phosphates, and peripheral tissue utilization of plasma glucose.