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, Cary R. Savage

Research output: Contribution to journalArticle

110 Citations (Scopus)

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).

Original languageEnglish (US)
Pages (from-to)1028-1037
Number of pages10
JournalObesity
Volume14
Issue number6
DOIs
StatePublished - Jun 1 2006

Fingerprint

Prader-Willi Syndrome
Hyperphagia
Meals
Prefrontal Cortex
Food
Eating
Amygdala
Weights and Measures
Control Groups
Obesity
Magnetic Resonance Imaging
Obsessive Behavior
Parahippocampal Gyrus
Inborn Genetic Diseases
Feeding Behavior
Motivation
Hippocampus

Keywords

  • Amygdala
  • Food motivation
  • Functional magnetic resonance imaging
  • Genetics
  • Prader-Willi syndrome

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

Cite this

Holsen, L. M., Zarcone, J. R., Brooks, W. M., Butler, M. G., Thompson, T. I., Ahluwalia, J. S., ... Savage, C. R. (2006). Neural mechanisms underlying hyperphagia in Prader-Willi syndrome. Obesity, 14(6), 1028-1037. https://doi.org/10.1038/oby.2006.118

Neural mechanisms underlying hyperphagia in Prader-Willi syndrome. / Holsen, Laura M.; Zarcone, Jennifer R.; Brooks, William M.; Butler, Merlin G.; Thompson, Travis I.; Ahluwalia, Jasjit S.; Nollen, Nicole L.; Savage, Cary R.

In: Obesity, Vol. 14, No. 6, 01.06.2006, p. 1028-1037.

Research output: Contribution to journalArticle

Holsen, LM, Zarcone, JR, Brooks, WM, Butler, MG, Thompson, TI, Ahluwalia, JS, Nollen, NL & Savage, CR 2006, 'Neural mechanisms underlying hyperphagia in Prader-Willi syndrome', Obesity, vol. 14, no. 6, pp. 1028-1037. https://doi.org/10.1038/oby.2006.118
Holsen LM, Zarcone JR, Brooks WM, Butler MG, Thompson TI, Ahluwalia JS et al. Neural mechanisms underlying hyperphagia in Prader-Willi syndrome. Obesity. 2006 Jun 1;14(6):1028-1037. https://doi.org/10.1038/oby.2006.118
Holsen, Laura M. ; Zarcone, Jennifer R. ; Brooks, William M. ; Butler, Merlin G. ; Thompson, Travis I. ; Ahluwalia, Jasjit S. ; Nollen, Nicole L. ; Savage, Cary R. / Neural mechanisms underlying hyperphagia in Prader-Willi syndrome. In: Obesity. 2006 ; Vol. 14, No. 6. pp. 1028-1037.
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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).",
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