Ghrelin system and GLP-1 as potential treatment targets for alcohol use disorder

Nov 10, 2024International review of neurobiology

Ghrelin and GLP-1 systems as possible treatment targets for alcohol use disorder

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Abstract

Ghrelin and glucagon-like peptide-1 (GLP-1) are associated with alcohol use disorder (AUD) and may serve as potential treatment targets.

Ghrelin increases alcohol intake in rodents and craving for alcohol in humans.
Suppression of the ghrelin receptor reduces alcohol-related responses in animal models of AUD.
Ghrelin receptor antagonism results in lower alcohol intake, less motivation to consume alcohol, and reduced reward from alcohol.
GLP-1 receptor agonists approved for treating type 2 diabetes and obesity also reduce alcohol intake and prevent relapse in preclinical studies.
In overweight patients with AUD, GLP-1 receptor agonists have been shown to decrease alcohol intake.
Genetic variations in the genes related to ghrelin and GLP-1 are associated with AUD and heavy alcohol consumption.

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Peptides of the gut-brain axis have gained recent attention as potential treatment targets for addiction. While the number of gut-brain peptides is vast, ghrelin and glucagon-like peptide-1 (GLP-1) have been suggested as important players. Ghrelin is traditionally considered an orexigenic peptide, but recent studies found that it increases alcohol intake in rodents and craving for alcohol in humans. Additionally, suppression of the ghrelin receptor attenuates alcohol-related responses in animal models reflecting alcohol use disorder (AUD). For instance, a lower alcohol intake, suppressed motivation to consume alcohol, and attenuated reward from alcohol is observed after ghrelin receptor antagonism treatment. On a similar note, a partial ghrelin receptor agonist prevents hangover symptoms in humans. When it comes to the anorexigenic peptide GLP-1, agonists of its receptor are approved to treat diabetes type 2 and obesity. Extensive preclinical studies have revealed that these GLP-1 receptor agonists reduce alcohol intake, suppress the motivation to consume alcohol, and prevent relapse drink, with effects tentatively associated with a reduced alcohol-induced reward. These preclinical findings have to some extent been varied in humans, as GLP-1 receptor agonists decrease alcohol intake in overweight patients with AUD. Furthermore, genetic variations in either the genes encoding for pre-pro-ghrelin, GHSR, GLP-1, or its receptor, are associated with AUD and heavy alcohol drinking. While central mechanisms appear to modulate the ability of either ghrelin or GLP-1 to regulate alcohol-related responses the exact mechanisms have not been defined. Taken together these preclinical and clinical data imply that gut-brain peptides participate in the addiction process and should be considered as potential targets for AUD treatment.

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Ghrelin system and GLP-1 as potential treatment targets for alcohol use disorder

Abstract

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