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Variations in a gene that regulates food intake are associated with anorexia nervosa

Anorexia Nervosa (AN) is a dramatic disease with a high degree of mortality. Family studies suggested a strong genetic component in AN. The authors demonstrate for the first time an association between a mutation in a gene, Agouti-related Protein (AgRP), and AN. AgRP stimulates food intake when injected into brains of rats and mice, because AgRP suppresses melanocortin receptor activity. Genetic studies in humans and mice demonstrated that decreased activity of melanocortin receptors is associated with obesity. The authors' finding suggests that the opposite occurs when there is increased melanocortin receptor activity: inadequate suppression of melanocortin receptors by (mutated) AgRP increases the susceptibility to develop AN.

ARTICLE: "Association between an agouti-related protein gene polymorphism and anorexia nervosa"

AUTHORS: T Vink, A Hinney, AA van Elburg, SHM van Goozen, LA Sandkuijl, RJ Sinke, BM Herpertz-Dahlmann, J Hebebrand, H Remschmidt, H van Engeland and RAH Adan

Rudolf Magnus Institute for Neurosciences, Utrecht University Medical Center, 3584 CG Utrecht, The Netherlands and Universities of Marburg and Aachen, Germany

Citation source: Molecular Psychiatry 2001 Volume 6, number 3, pages 325-328.

For further information on this work, please contact Dr. Roger A.H. Adan, Rudolf Magnus Institute for Neurosciences, Utrecht University Medical Center, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands; Tel: 31 30 253 8517; Fax: 31 30 253 8859 or 9032; e-mail: r.a.h.adan@med.uu.nl

Molecular Psychiatry is published by the Nature Publishing Group. http://www.nature.com/mp

Editor: Julio Licinio, M.D.; phone: +1 310 206-6207; FAX: +1 310 825-6407; e-mail: licinio@ucla.edu
Editorial assistant: Ms. Ava Martin; phone: +1 310 206-6739; FAX: +1 310 825-6407; e-mail: molecularpsychiatry@mednet.ucla.edu

For a copy of this article, please contact Ms. Martin.

PLEASE CITE MOLECULAR PSYCHIATRY AS THE SOURCE OF THIS MATERIAL.

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