Neurobiological Mechanisms and Therapeutic Potential of Glucagon-like Peptide-1 Receptor Agonists in Binge Eating Disorder: A Narrative Review
Issued Date
2025-11-01
Resource Type
ISSN
16616596
eISSN
14220067
Scopus ID
2-s2.0-105023092417
Journal Title
International Journal of Molecular Sciences
Volume
26
Issue
22
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences Vol.26 No.22 (2025)
Suggested Citation
Tongta S., Sungkaworn T., Pathomthongtaweechai N. Neurobiological Mechanisms and Therapeutic Potential of Glucagon-like Peptide-1 Receptor Agonists in Binge Eating Disorder: A Narrative Review. International Journal of Molecular Sciences Vol.26 No.22 (2025). doi:10.3390/ijms262210974 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/113380
Title
Neurobiological Mechanisms and Therapeutic Potential of Glucagon-like Peptide-1 Receptor Agonists in Binge Eating Disorder: A Narrative Review
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Author's Affiliation
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Abstract
Binge eating disorder (BED) is a prevalent eating disorder lacking adequate pharmacological interventions. This review examines the therapeutic potential of glucagon-like peptide-1 receptor agonists (GLP-1RAs), medications approved for type 2 diabetes and obesity now being investigated for eating disorders through their modulation of metabolic and reward pathways. A narrative review was conducted using PubMed/MEDLINE, through May 2025, to examine GLP-1RA effects on BED, including preclinical and clinical studies, mechanistic investigations, and relevant reviews. GLP-1 receptors (GLP-1Rs) are expressed in hypothalamic nuclei, regulating energy homeostasis and mesolimbic circuits controlling food reward. Preclinical studies demonstrate that GLP-1RAs reduce food-seeking behavior, suppress dopamine signaling in reward circuits, and modulate neural transmission in key brain regions. These effects extend beyond appetite suppression to directly modify reward processing underlying compulsive eating. Emerging clinical evidence with semaglutide and liraglutide report reductions in binge eating episodes, decreased food cravings, and improved symptom scores. However, current studies remain small-scale with methodological limitations, and translating findings from animal models to human eating disorder complexity presents significant challenges. This review integrates preclinical and clinical evidence demonstrating that GLP-1RAs modulate both metabolic and reward pathways. By elucidating the underlying neurobiological mechanisms, GLP-1RAs may offer advantages over current symptom-focused therapies for BED.