Melanocortin System and Eating Disorders

Authors

  • ROGER A.H. ADAN,

    Corresponding author
    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • JACQUELIEN J.G. HILLEBRAND,

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • CORINE De RIJKE,

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • WOUTER NIJENHUIS,

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • TOM VINK,

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • KEITH M. GARNER,

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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  • MARTIEN J.H. KAS

    1. Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Utrecht, the Netherlands
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Address for correspondence: Roger A.H. Adan, Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Universiteitsweg 100, 3584 CG Utrecht, the Netherlands. Voice: +31 30 2538517; fax: +31 30 2539032. r.a.h.adan@med.uu.nl

Abstract

Abstract: The melanocortin (MC) system is involved in the regulation of energy balance and in the development of obesity. Here we briefly review why we became interested in investigating whether the MC system — more particularly, the increased activity of the MC system — is also involved in disorders of negative energy balance. We provide evidence that suppression of increased MC receptor activity by treatment with the inverse agonist agouti-related peptide (AgRP) (83–132) rescues rats exposed to an animal model known as activity-based anorexia. Furthermore, we found a polymorphism, Ala67Thr AgRP, that was observed more frequently in anorexia nervosa.

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