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Glucagon-like Receptor Agonists01:24

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Related Experiment Video

Updated: Jul 10, 2026

Assessing Activity-based Anorexia in Mice
08:26

Assessing Activity-based Anorexia in Mice

Published on: May 14, 2018

GLP-1 Receptor Agonism Exacerbates Activity-Based Anorexia in Mice.

Amit Thakar1, Travis E Brown1, Shane T Hentges1

  • 1Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, Washington, USA.

The International Journal of Eating Disorders
|July 9, 2026
PubMed
Summary

Glucagon-like peptide-1 receptor (GLP-1R) agonists worsen anorexia nervosa outcomes by increasing weight loss and reducing food intake in a rodent model. These findings caution against using GLP-1R agonists in individuals prone to restrictive eating behaviors.

Keywords:
GLP‐1 receptor agonistGLP‐1 receptor antagonistactivity‐based anorexiafood intakemicemotivated behaviorrestricted feedingweight losswheel‐running

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Published on: May 24, 2018

Area of Science:

  • Neuroscience
  • Endocrinology
  • Eating Disorders Research

Background:

  • Glucagon-like peptide-1 receptor (GLP-1R) agonists are known to reduce food intake and body weight.
  • Preclinical data suggested GLP-1R agonists might mitigate hyperactivity and reward-seeking behavior, potentially benefiting anorexia nervosa (AN).
  • Activity-based anorexia (ABA) is a rodent model used to study AN pathology, characterized by hyperactivity and weight loss.

Purpose of the Study:

  • To investigate the effects of GLP-1R agonists on weight loss and hyperactivity in a rodent model of activity-based anorexia (ABA).
  • To determine if GLP-1R agonism could attenuate compulsive-like hyperactivity or worsen outcomes in ABA.

Main Methods:

  • Female mice were subjected to ABA conditions with running wheel access and restricted feeding.
  • Systemic administration of a GLP-1R agonist, antagonist, or vehicle was performed daily before food presentation.
  • Key parameters monitored included weight loss, food intake, and wheel running activity.

Main Results:

  • GLP-1R agonist treatment significantly exacerbated weight loss in the ABA model.
  • This worsening was attributed to further suppressed food intake, with no change in wheel running activity.
  • Pharmacological blockade of GLP-1R signaling did not affect ABA parameters compared to controls.

Conclusions:

  • GLP-1R agonism worsens outcomes in an animal model of anorexia nervosa, contrary to initial hypotheses.
  • Endogenous GLP-1 signaling does not appear to play a significant role in ABA pathology.
  • Caution is advised for using GLP-1R agonists in individuals at risk for AN due to potential exacerbation of weight loss and reduced food intake.