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The glucagon-like peptide 1 receptor agonist liraglutide attenuates the reinforcing properties of alcohol in rodents.

Journal article
Authors Daniel Vallöf
Paola Maccioni
Giancarlo Colombo
Minja Mandrapa
Julia Winsa Jörnulf
Emil Egecioglu
Jörgen Engel
Elisabeth Jerlhag
Published in Addiction Biology
Volume 21
Issue 2
Pages 422–437
ISSN 1355-6215
Publication year 2016
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 422–437
Language en
Links dx.doi.org/10.1111/adb.12295
Keywords Addictive behaviours;dependence;reward
Subject categories Pharmacology

Abstract

The incretin hormone, glucagon-like peptide 1 (GLP-1), regulates gastric emptying, glucose-dependent stimulation of insulin secretion and glucagon release, and GLP-1 analogs are therefore approved for treatment of type II diabetes. GLP-1 receptors are expressed in reward-related areas such as the ventral tegmental area and nucleus accumbens, and GLP-1 was recently shown to regulate several alcohol-mediated behaviors as well as amphetamine-induced, cocaine-induced and nicotine-induced reward. The present series of experiments were undertaken to investigate the effect of the GLP-1 receptor agonist, liraglutide, on several alcohol-related behaviors in rats that model different aspects of alcohol use disorder in humans. Acute liraglutide treatment suppressed the well-documented effects of alcohol on the mesolimbic dopamine system, namely alcohol-induced accumbal dopamine release and conditioned place preference in mice. In addition, acute administration of liraglutide prevented the alcohol deprivation effect and reduced alcohol intake in outbred rats, while repeated treatment of liraglutide decreased alcohol intake in outbred rats as well as reduced operant self-administration of alcohol in selectively bred Sardinian alcohol-preferring rats. Collectively, these data suggest that GLP-1 receptor agonists could be tested for treatment of alcohol dependence in humans.

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