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Elevated plasma ghrelin levels in Prader–Willi syndrome

Nature Medicine volume 8, pages 643–644 (2002)Cite this article

To the editor

Recent advances have begun to clarify the pathogenesis of genetic obesity in humans. Mutations that affect signaling by leptin and melanocortins were hypothesized to contribute to human obesity based on their important roles in body-weight regulation in rodent models, and compelling support for this hypothesis now exists1,2,3. Ghrelin is a novel enteric hormone4 that increases food intake, body weight and growth-hormone (GH) secretion as potently as any known peptide4,5,6,7. As the only known circulating orexigen, ghrelin is implicated in meal-time hunger8 and body-weight regulation in rodents5,6 and humans9,10. However, previous studies have not investigated the hypothesis that ghrelin hypersecretion might contribute to genetic obesity.

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Figure 1: Obesity from PWS is associated with high circulating ghrelin levels.

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Authors and Affiliations

  1. Department of Medicine, VA Puget Sound Health Care System and Harborview Medical Center University of Washington, Seattle, Washington, USA

    David E. Cummings, Karen E. Foster, R. Scott Frayo, Michael W. Schwartz & David S. Weigle

  2. Service de Medecine et Nutrition, Hotel-Dieu EA 3502 Paris VI University, France

    Karine Clement & Arnaud Basdevant

  3. Department of Medicine, Oregon Health & Science University, Portland, Oregon, USA

    Jonathan Q. Purnell

  4. Department of Medicine and Diabetes Center University of California, San Francisco, California, USA

    Christian Vaisse

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Cummings, D., Clement, K., Purnell, J. et al. Elevated plasma ghrelin levels in Prader–Willi syndrome. Nat Med 8, 643–644 (2002). https://doi.org/10.1038/nm0702-643

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