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Updated: May 16, 2025

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
Comprehensive insights into emerging advances in the Neurobiology of anorexia
Liwei Mao1, Lian Wang1, Zhihai Huang2
1Department of Neurology, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA 30912, USA.
Background:
Anorexia is a complex eating disorder influenced by genetic, environmental, psychological, and socio-cultural factors. Research into its molecular mechanisms and neural circuits has deepened our understanding of its pathogenesis. Recent advances in neuroscience, molecular biology, and genetics have revealed key molecular and neural circuit mechanisms underlying anorexia.
Aim Of Review:
Clarify the peripheral and central molecular mechanisms regulating various types of anorexia, identify key cytokines and neural circuits, and propose new strategies for its treatment. Key scientific concepts of review: Anorexia animal models, including activity-induced, genetic mutation, and inflammation-induced types, are explored for their relevance to studying the disorder. Anorexic behavior is regulated by cytokines, hormones (like GDF15, GLP-1, and leptin), and neural circuits such as AgRP, serotonergic, dopaminergic, and glutamatergic pathways. Disruptions in these pathways, including GABAergic signaling in AgRP neurons and 5-HT2C and D2 receptors, contribute to anorexia. Potential therapies target neurotransmitter receptors, ghrelin receptors, and the GDF15-GFRAL pathway, offering insights for treating anorexia, immune responses, and obesity.
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