Molecular metabolismOct 6, 2026

Specific brain neurons help control nausea caused by incretin hormones but do not affect appetite or weight loss

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 7, 2026

Abstract

Liraglutide activates parabrachial CGRP neurons, which is required for its aversive effects.

Liraglutide is associated with decreased food intake and weight loss.
Activation of parabrachial CGRP neurons is necessary for liraglutide-induced aversion, but not for its effects on appetite or weight.
Glucose-dependent insulinotropic polypeptide receptor (GIPR) agonism can reduce liraglutide-induced taste avoidance and CGRP neuron activation.
The anti-emetic drug ondansetron also alleviates liraglutide-induced conditioned taste avoidance without impacting its appetite-suppressing effects.
Distinct neural mechanisms mediate the aversive and appetite-suppressing effects of liraglutide.

Simplified

Incretin mimetics such as the glucagon-like peptide-1 receptor agonist (GLP-1RA) liraglutide cause decreased food intake, weight loss, and aversion. Here, we examined the extent to which parabrachial calcitonin gene-related peptide (CGRP) neurons contribute to these effects. Further, we assessed whether glucose-dependent insulinotropic polypeptide receptor (GIPR) agonism alters liraglutide-induced behavior and CGRP neuron activity. We found that liraglutide activates parabrachial CGRP neurons and that this is required for liraglutide-induced aversion, but not anorexia or weight loss. Additionally, treatment with a GIPR agonist (GIPRA) or the well-established anti-emetic drug ondansetron ameliorated liraglutide-induced conditioned taste avoidance (CTA) and CGRP neuron activation without affecting acute liraglutide-induced feeding suppression. Taken together, our findings demonstrate that the aversive and anorexigenic effects of liraglutide are mediated by distinct neural mechanisms that can be separably manipulated. Our findings also highlight GIPR agonism as an emerging anti-aversive approach to GLP-1RA-induced malaise while maintaining the beneficial metabolic effects.

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Specific brain neurons help control nausea caused by incretin hormones but do not affect appetite or weight loss

Abstract

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