Hepatic metabolism in patients with alcoholic cirrhosis.
Fuel homeostasis was studied in 15 patients with hepatic cirrhosis who previously had sustained upper gastrointestinal hemorrhage secondary to portal hypertension. By combining substrate arteriovenous concentration differences with measured hepatic blood flow rates, the exchange rates of metabolites across the liver was calculated. Hepatic extraction of acetoacetate, beta-hydroxybutyrate, lactate, pyruvate, analine, and glycerol was studied. After an overnight fast, splanchnic glucose production in 15 cirrhotic patients was diminished markedly. Despite reduced total glucose production, there was no decrease in hepatic gluconeogenesis; instead, there was increased glucose formation from amino acids, glycerol, lactate, and pyruvate. In patients with hepatic cirrhosis, the liver does not produce as much glucose as does a normal liver; the failing cirrhotic liver is capable of maintaining fuel homeostasis by increased ketone-body production.
D000596:Amino Acids / Q000378:metabolism; D005943:Gluconeogenesis; D005947:Glucose / Q000096:biosynthesis; D005990:Glycerol / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007657:Ketone Bodies / Q000096:biosynthesis; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation; D008104:Liver Cirrhosis, Alcoholic / Q000378:metabolism*; D011773:Pyruvates / Q000378:metabolism
D000596:Amino Acids; D007657:Ketone Bodies; D007773:Lactates; D011773:Pyruvates; D005947:Glucose; D005990:Glycerol