Steven B. Heymsfield, Nicole M. Avena, Leslie Baier, Phillip Brantley, George A. Bray, Lisa C. Burnett, Merlin G. Butler, Daniel J. Driscoll, Dieter Egli, Joel Elmquist, Janice L. Forster, Anthony P. Goldstone, Linda M. Gourash, Frank L. Greenway, Joan C. Han, James G. Kane, Rudolph L. Leibel, Ruth J.F. Loos, Ann O. Scheimann, Christian L. Roth, Randy J. Seeley, Val Sheffield, Maïthé Tauber, Christian Vaisse, Liheng Wang, Robert A. Waterland, Rachel Wevrick, Jack A. Yanovski andAndrew R. Zinn
Obesity Volume 22, Issue S1, pages S1–S17, February 2014
Hyperphagia is a central feature of inherited disorders (e.g., Prader–Willi Syndrome) in which obesity is a primary phenotypic component. Hyperphagia may also contribute to obesity as observed in the general population, thus raising the potential importance of common underlying mechanisms and treatments. Substantial gaps in understanding the molecular basis of inherited hyperphagia syndromes are present as are a lack of mechanistic of mechanistic targets that can serve as a basis for pharmacologic and behavioral treatments.
Design and Methods
International conference with 28 experts, including scientists and caregivers, providing presentations, panel discussions, and debates.
The reviewed collective research and clinical experience provides a critical body of new and novel information on hyperphagia at levels ranging from molecular to population. Gaps in understanding and tools needed for additional research were identified.
This report documents the full scope of important topics reviewed at a comprehensive international meeting devoted to the topic of hyperphagia and identifies key areas for future funding and research.