Effects of lactate infusion on hepatic gluconeogenesis and glycogenolysis.

Détails

ID Serval
serval:BIB_8485471F7B24
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Effects of lactate infusion on hepatic gluconeogenesis and glycogenolysis.
Périodique
Clinical Physiology
Auteur(s)
Haesler E., Schneiter P., Temler E., Jéquier E., Tappy L.
ISSN
0144-5979[print], 0144-5979[linking]
Statut éditorial
Publié
Date de publication
1995
Volume
15
Numéro
6
Pages
581-595
Langue
anglais
Notes
Publication types: Clinical Trial ; Controlled Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
Résumé
Endogenous glucose production rate (EGPR) remains constant when lactate is infused in healthy humans. A decrease of glycogenolysis or of gluconeogenesis from endogenous precursors or a stimulation of glycogen synthesis, may all be involved; This autoregulation does not depend on changes in glucoregulatory hormones. It may be speculated that alterations in basal sympathetic tone may be involved. To gain insights into the mechanisms responsible for autoregulation of EGPR, glycogenolysis and gluconeogenesis were measured, with a novel method (based on the prelabelling of endogenous glycogen with 13C glucose, and determination of hepatic 13C glycogen enrichment from breath 13CO2 and respiratory gas exchanges) in healthy humans infused with lactate or saline. These measurements were performed with or without beta-adrenergic receptor blockade (propranolol). Infusion of lactate increased energy expenditure, but did not increase EGPR; the relative contributions of gluconeogenesis and glycogenolysis to EGPR were also unaltered. This indicates that autoregulation is attained, at least in part, by inhibition of gluconeogenesis from endogenous precursors. beta-adrenergic receptor blockade alone (with propranolol) did not alter EGPR, glycogenolysis or gluconeogenesis. During infusion of lactate, propranolol decreased the thermic effect of lactate but EGPR remained constant. This indicates that alterations of beta-adrenergic activity is not required for autoregulation of EGPR.
Mots-clé
Adrenergic beta-Antagonists/pharmacology, Adult, Blood Glucose/metabolism, Body Temperature Regulation/drug effects, Calorimetry, Indirect, Carbon Dioxide/metabolism, Energy Metabolism/physiology, Gluconeogenesis/drug effects, Heart Rate/drug effects, Heart Rate/physiology, Humans, Infusions, Intravenous, Lactates/administration &amp, dosage, Lactates/pharmacokinetics, Lactic Acid, Liver/drug effects, Liver/metabolism, Liver Glycogen/metabolism, Male, Oxidation-Reduction, Propranolol/pharmacology
Pubmed
Web of science
Création de la notice
24/01/2008 14:36
Dernière modification de la notice
03/03/2018 18:55
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