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 in | Metabolism, clinical and experimental Vol. 48; no. 10; pp. 1260 - 1266 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.10.1999
Elsevier |
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Online Access | Get full text |
ISSN | 0026-0495 1532-8600 |
DOI | 10.1016/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. |
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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 |
Author_xml | – sequence: 1 givenname: Philippe surname: Schneiter fullname: Schneiter, Philippe organization: Institut de physiologie, Université de Lausanne, Lausanne, Switzerland – sequence: 2 givenname: Michel surname: Gillet fullname: Gillet, Michel organization: Institut de physiologie, Université de Lausanne, Lausanne, Switzerland – sequence: 3 givenname: René surname: Chioléro fullname: Chioléro, René organization: Institut de physiologie, Université de Lausanne, Lausanne, Switzerland – sequence: 4 givenname: Eric surname: Jéquier fullname: Jéquier, Eric organization: Institut de physiologie, Université de Lausanne, Lausanne, Switzerland – sequence: 5 givenname: Luc surname: Tappy fullname: Tappy, Luc organization: Institut de physiologie, Université de Lausanne, Lausanne, Switzerland |
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CitedBy_id | crossref_primary_10_1371_journal_pone_0109134 crossref_primary_10_1134_S1990519X09060108 crossref_primary_10_1134_S1990519X15020030 crossref_primary_10_1152_ajpendo_2001_281_3_E413 crossref_primary_10_1371_journal_pone_0217751 crossref_primary_10_1093_ajcn_84_6_1374 crossref_primary_10_2337_dc12_0540 crossref_primary_10_3945_ajcn_2008_27296 crossref_primary_10_1038_sj_ijo_0801386 crossref_primary_10_1152_ajpendo_00542_2012 crossref_primary_10_3945_ajcn_2008_27336 crossref_primary_10_1016_j_etp_2013_12_001 crossref_primary_10_3945_ajcn_2010_29566 crossref_primary_10_1093_jn_nxz274 crossref_primary_10_1017_S0007114509992819 crossref_primary_10_1016_j_eclnm_2010_09_001 crossref_primary_10_1113_expphysiol_2009_050690 crossref_primary_10_1007_s12072_013_9458_8 crossref_primary_10_2337_diabetes_54_7_1907 |
Cites_doi | 10.1172/JCI106016 10.1079/BJN19740060 10.2337/diacare.21.1.S5 10.1007/BF00279918 10.1016/S0950-351X(05)80163-6 10.1172/JCI118379 10.1016/0026-0495(95)90261-9 10.1172/JCI119775 10.1007/BF01222973 10.1172/JCI117602 10.1002/hep.1840180115 10.1007/s001250050745 10.1177/0148607190014006563 10.1093/ajcn/47.4.608 10.1172/JCI115340 10.1055/s-2007-1010889 10.1016/0026-0495(85)90059-9 10.1007/s001250050141 10.1002/hep.1840180210 10.2337/diabetes.39.11.1381 |
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Keywords | Endocrinopathy Human Pathogenesis Liver Hepatic disease Glucose Metabolism Cirrhosis Food intake Digestive diseases Adult Complication Impaired glucose tolerance Comparative study |
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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 |
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