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Updated: Jan 29, 2026

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
Neuroendocrine dysregulation and the growth hormone-IGF-1 axis in anorexia nervosa
Pouneh K Fazeli1, Anne Klibanski2
1a Neuroendocrine Unit, Bulfinch 457B, Massachusetts General Hospital & Harvard Medical School, Boston, MA 02114, USA.
Abstract:
Anorexia nervosa is a common psychiatric disorder characterized by extreme, self-induced starvation and is associated with a number of medical complications, including significant loss of bone mass. Disruption of the hypothalamic-pituitary axis has been demonstrated in anorexia nervosa and contributes to both loss of established bone mass in adults and failure to accrue normal bone mass in adolescents. Anorexia nervosa is associated with the development of a state of acquired growth hormone (GH) resistance, characterized by low IGF-1 and elevated GH levels, which may be mediated in part by FGF-21. Administration of supraphysiologic recombinant human GH does not result in an increase in markers of bone formation. However, treatment with recombinant human IGF-1, in combination with an oral contraceptive, increases markers of bone formation as well as bone mineral density, and may be a novel way to treat the bone loss associated with anorexia nervosa.
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