Original Article
Obesity Research (2006) 14, 1028–1037; doi: 10.1038/oby.2006.118
Neural Mechanisms Underlying Hyperphagia in Prader-Willi Syndrome*
Laura M. Holsen*,†, Jennifer R. Zarcone‡, William M. Brooks*,¶, Merlin G. Butler**, Travis I. Thompson††, Jasjit S. Ahluwalia‡‡, Nicole L. Nollen
and Cary R. Savage*,§
- *Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas City, Kansas;
- †Waisman Center and Waisman Laboratory for Brain Imaging and Behavior, University of Wisconsin–Madison, Madison, Wisconsin;
- ‡Department of Pediatrics and Strong Center for Developmental Disabilities, University of Rochester Medical Center, Rochester, New York;
- §Department of Psychiatry and Behavioral Sciences, University of Kansas Medical Center, Kansas
- ¶Department of Neurology, University of Kansas Medical Center, Kansas
Department of Preventive Medicine, University of Kansas Medical Center, Kansas- **Children's Mercy Hospital, Kansas City, Missouri;
- ††Department of Pediatrics and Center for Neurobehavioral Development, School of Medicine, University of Minnesota, Minneapolis, Minnesota
- ‡‡Office of Clinical Research, Academic Health Center, University of Minnesota, Minneapolis, Minnesota.
Correspondence: Cary R. Savage Hoglund Brain Imaging Center, Mail Stop 1052, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160. E-mail: csavage@kumc.edu
*The costs of publication of this article were defrayed, in part, by the payment of page charges. This article must, therefore, be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 10 August 2005; Revised 0000; Accepted 24 March 2006.
Abstract
Objective: Prader-Willi syndrome (PWS) is a genetic disorder associated with developmental delay, obesity, and obsessive behavior related to food consumption. The most striking symptom of PWS is hyperphagia; as such, PWS may provide important insights into factors leading to overeating and obesity in the general population. We used functional magnetic resonance imaging to study the neural mechanisms underlying responses to visual food stimuli, before and after eating, in individuals with PWS and a healthy weight control (HWC) group.
Research Methods and Procedures: Participants were scanned once before (pre-meal) and once after (post-meal) eating a standardized meal. Pictures of food, animals, and blurred control images were presented in a block design format during acquisition of functional magnetic resonance imaging data.
Results: Statistical contrasts in the HWC group showed greater activation to food pictures in the pre-meal condition compared with the post-meal condition in the amygdala, orbitofrontal cortex, medial prefrontal cortex (medial PFC), and frontal operculum. In comparison, the PWS group exhibited greater activation to food pictures in the post-meal condition compared with the pre-meal condition in the orbitofrontal cortex, medial PFC, insula, hippocampus, and parahippocampal gyrus. Between-group contrasts in the pre- and post-meal conditions confirmed group differences, with the PWS group showing greater activation than the HWC group after the meal in food motivation networks.
Discussion: Results point to distinct neural mechanisms associated with hyperphagia in PWS. After eating a meal, the PWS group showed hyperfunction in limbic and paralimbic regions that drive eating behavior (e.g., the amygdala) and in regions that suppress food intake (e.g., the medial PFC).
Keywords:
amygdala, Prader-Willi syndrome, functional magnetic resonance imaging, food motivation, genetics
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