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1 Department of Nutritional
Sciences,
Accurate
quantification of gluconeogenic flux following alcohol ingestion in
overnight-fasted humans has yet to be reported. [2-13C1]glycerol,
[U-13C6]glucose,
[1-2H1]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 glucose production, and intrahepatic
gluconeogenic precursor availability. Gluconeogenesis decreased 45%
vs. the placebo (0.56 ± 0.05 to 0.44 ± 0.04 mg · kg
1 · min1
vs. 0.44 ± 0.05 to 0.63 ± 0.09 mg · kg1 · min1
, respectively, P < 0.05) in the
5 h after alcohol ingestion, and total gluconeogenic flux was lower
after alcohol compared with placebo. Glycogenolysis fell over time
after both the alcohol and placebo cocktails, from 1.46-1.47
mg · kg1 · min1
to 1.35 ± 0.17 mg · kg1 · min1
(alcohol) and 1.26 ± 0.20 mg · kg1 · min1,
respectively (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 · kg1 · min1
(P < 0.05 vs. baseline), but did not
change following the placebo. Estimated intrahepatic gluconeogenic
precursor availability decreased 61% following alcohol consumption
(P < 0.05 vs. baseline) 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 decrease in availability
of gluconeogenic precursors but a smaller effect on glucose production
and no effect on plasma glucose concentrations. Thus inhibition of flux
into the gluconeogenic precursor pool is compensated by changes in
glycogenolysis, the fate of triose-phosphates, and peripheral tissue
utilization of plasma glucose.
mass isotopomer distribution analysis; glucose production; stable isotopes
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