Hepatic nonoxidative disposal of an oral glucose meal in patients with liver cirrhosis

Metabolism. 1999 Oct;48(10):1260-6. doi: 10.1016/s0026-0495(99)90265-2.


Seven patients with liver cirrhosis and five healthy subjects were studied over 4 hours after ingestion of a glucose meal to determine whether alterations of hepatic nonoxidative glucose disposal participate in the pathogenesis of impaired glucose tolerance. Hepatic uridyl-diphosphoglucose (UDPG) turnover was calculated from the isotopic enrichment of urinary acetaminophen glucuronide during continuous infusion of 13C-galactose and used as an index of hepatic glycogen synthesis. Patients with cirrhosis had postprandial hyperglycemia and decreased glucose clearance, but hepatic UDPG turnover was not altered (1.84 +/- 0.29 mg/kg fat-free mass min v 1.76 +/- 0.15 in controls, nonsignificant). It is concluded that hepatic postprandial glycogen synthesis is unaltered in patients with advanced cirrhosis, demonstrating important hepatic functional reserve.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Carbon Isotopes
  • Eating
  • Female
  • Galactose / metabolism
  • Glucose / metabolism*
  • Glucose Intolerance / etiology
  • Glucose Intolerance / physiopathology
  • Humans
  • Hyperglycemia / etiology
  • Hyperglycemia / metabolism
  • Intestinal Absorption
  • Liver / metabolism*
  • Liver Cirrhosis / etiology
  • Liver Cirrhosis / metabolism*
  • Liver Glycogen / biosynthesis
  • Male
  • Middle Aged
  • Postprandial Period
  • Prothrombin Time
  • Reference Values
  • Uridine Diphosphate Glucose / metabolism


  • Carbon Isotopes
  • Liver Glycogen
  • Glucose
  • Uridine Diphosphate Glucose
  • Galactose