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Updated: Jun 27, 2026

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
Leptin-mediated neuroendocrine alterations in anorexia nervosa: somatic and behavioral implications
Timo D Müller1, Manuel Föcker, Kristian Holtkamp
1Department of Child and Adolescent Psychiatry and Psychotherapy, University of Duisburg-Essen, Virchowstrasse 174, 45147 Essen, Germany.
Abstract:
Hypoleptinemia is a key endocrinological feature of anorexia nervosa (AN). Several symptoms in acute AN are related to the low circulating leptin levels including amenorrhea and semi-starvation-induced hyperactivity. The drop in leptin levels results from the loss of fat mass; once leptin levels fall below specific thresholds the hypothalamic-pituitary-gonadal and -thyroid axes are down-regulated; in contrast, the hypothalamic-pituitary-adrenal axis is up-regulated. Hypoleptinemia is the major signal underlying both somatic and behavioral adaptations to starvation. Because the mechanisms involved in this adaptation are similar in rodents and humans, rodent models can be used to investigate the relevant central pathways which underly the respective starvation-induced symptoms. During therapeutically induced weight gain, leptin levels can intermittently increase above normal concentrations. This hyperleptinemia could predispose to renewed weight loss.
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