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

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) tu...

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Published inMetabolism, clinical and experimental Vol. 48; no. 10; pp. 1260 - 1266
Main Authors Schneiter, Philippe, Gillet, Michel, Chioléro, René, Jéquier, Eric, Tappy, Luc
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.10.1999
Elsevier
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ISSN0026-0495
1532-8600
DOI10.1016/S0026-0495(99)90265-2

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Abstract 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.
AbstractList 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.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.
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.
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.
Author Tappy, Luc
Schneiter, Philippe
Jéquier, Eric
Gillet, Michel
Chioléro, René
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Issue 10
Keywords Endocrinopathy
Human
Pathogenesis
Liver
Hepatic disease
Glucose
Metabolism
Cirrhosis
Food intake
Digestive diseases
Adult
Complication
Impaired glucose tolerance
Comparative study
Language English
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Snippet 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...
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SubjectTerms Adult
Biological and medical sciences
Carbon Isotopes
Eating
Female
Galactose - metabolism
Gastroenterology. Liver. Pancreas. Abdomen
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
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Middle Aged
Other diseases. Semiology
Postprandial Period
Prothrombin Time
Reference Values
Uridine Diphosphate Glucose - metabolism
Title Hepatic nonoxidative disposal of an oral glucose meal in patients with liver cirrhosis
URI https://dx.doi.org/10.1016/S0026-0495(99)90265-2
https://www.ncbi.nlm.nih.gov/pubmed/10535388
https://www.proquest.com/docview/69210374
Volume 48
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