Effects of adrenergic blockade on hepatic glucose production during ethanol administration.

Détails

ID Serval
serval:BIB_CC766DEF2F68
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Effects of adrenergic blockade on hepatic glucose production during ethanol administration.
Périodique
Clinical Physiology
Auteur(s)
Delarue J., Schneiter P., Henry S., Cayeux C., Haesler E., Jéquier E., Tappy L.
ISSN
0144-5979[print], 0144-5979[linking]
Statut éditorial
Publié
Date de publication
1997
Volume
17
Numéro
5
Pages
509-521
Langue
anglais
Notes
Publication types: Clinical Trial ; Controlled Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
Résumé
Acute ethanol administration stimulates sympathetic nervous system activity. The present study was designed to determine whether this sympathetic activation affects glycogenolysis and total hepatic glucose production (HGP) during ethanol-induced inhibition of gluconeogenesis. Nineteen volunteers participated in four protocols. Two protocols aimed to study--using combined infusion of [6,6-2H2]glucose and [U-13C]glucose, VCO2 and 13CO2 measurements--the effects of ethanol infusion alone (n = 10) or with propranolol (n = 6) or phentolamine infusion (n = 4) on HGP, glucose disposal (Rd), glucose oxidation [13C]Glcox and non-oxidative glucose disposal (NOGD = Rd - [13C]Glcox). The fourth protocol assessed the effects of saline infusion alone on HGP. Using ethanol, HGP decreased by 23%, Rd by 20% and glycaemia by 9% (all P < 0.001); heart rate increased by 10%, whereas blood pressure remained unchanged. The effects were not observed with saline, except a slight (10%) decrease in HGP (P < 0.01 vs. ethanol). Ethanol did not affect [13C]Glcox but decreased NOGD by 73% (P < 0.001). Propranolol or phentolamine did not alter any of the effects of ethanol on glucose metabolism, but decreased mean arterial pressure. Propranolol prevented the ethanol-induced increase in heart rate. In conclusion, ethanol decreased blood glucose by decreasing HGP, presumably by inhibiting gluconeogenesis. Sympathetic activation prevented the decrease in blood pressure produced by ethanol but did not stimulate glycogenolysis.
Mots-clé
Adrenergic Antagonists/pharmacology, Adult, Blood Glucose/metabolism, Blood Pressure/drug effects, Blood Pressure/physiology, Ethanol/blood, Ethanol/toxicity, Fatty Acids, Nonesterified/blood, Glucagon/blood, Gluconeogenesis/drug effects, Glucose/biosynthesis, Glucose/metabolism, Heart Rate/drug effects, Heart Rate/physiology, Humans, Insulin/blood, Liver/drug effects, Liver/metabolism, Liver Glycogen/metabolism, Male, Phentolamine/pharmacology, Propranolol/pharmacology, Sympathetic Nervous System/drug effects, Sympathetic Nervous System/physiology
Pubmed
Web of science
Création de la notice
24/01/2008 14:36
Dernière modification de la notice
03/03/2018 21:28
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