HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shapira, N A Articles by Liu, Y Search for Related Content PubMed PubMed Citation Articles by Shapira, N A Articles by Liu, Y

Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI

¹ Department of Psychiatry, University of Florida, Gainesville, FL, USA
² Department of Pediatrics, University of Florida, Gainesville, FL, USA
³ Department of Psychiatry & Behavioral Sciences, University of Washington, Seattle, WA, USA

Correspondence to:
Correspondence to:
Dr N A Shapira
P.O. Box 100256, Gainesville, FL 32610–0256, USA; shapira{at}psychiatry.ufl.edu

ABSTRACT
The neurobiology relating to the insatiable appetite observed in Prader-Willi syndrome (PWS) has not been fully characterised. Two functional magnetic resonance imaging (fMRI) scans were performed on each of three adults with PWS. The scans were carried out pre- and post-treatment with the antiepileptic topiramate, which had little effect on body weight and appetite in these subjects. Subjects fasted overnight and drank a 75 g dextrose solution prior to fMRI scans for measurement of brain activation levels during/after glucose ingestion. Following glucose administration, there was a significant delay in activation at the hypothalamus and other brain regions associated with satiety compared with previous data on obese volunteers. These regions include the insula, ventromedial prefrontal cortex, and nucleus accumbens. Individuals with PWS showed a mean latency of 24 min while in a previous study obese volunteers had shown a latency of 15 min and lean volunteers a latency of 10 min in the hypothalamus. Our results provide evidence towards a satiety dysfunction in the central nervous system of PWS patients.

Abbreviations: EPI, echo planar imaging; fMRI, functional magnetic resonance imaging; PWS, Prader-Willi syndrome; ROI, region of interest; TCA, temporal clustering analysis

Keywords: brain activation; fMRI; hypothalamus; Prader-Willi syndrome; satiety

This article has been cited by other articles:

				J. L Miller, G A. James, A. P Goldstone, J. A Couch, G. He, D. J Driscoll, and Y. Liu Enhanced activation of reward mediating prefrontal regions in response to food stimuli in Prader-Willi syndrome J. Neurol. Neurosurg. Psychiatry, June 1, 2007; 78(6): 615 - 619. [Abstract] [Full Text] [PDF]

				S. E. Kim, D.-K. Jin, S. S. Cho, J.-H. Kim, S. D. Hong, K. H. Paik, Y. J. Oh, A. H. Kim, E. K. Kwon, and Y. H. Choe Regional Cerebral Glucose Metabolic Abnormality in Prader-Willi Syndrome: A 18F-FDG PET Study Under Sedation J. Nucl. Med., July 1, 2006; 47(7): 1088 - 1092. [Abstract] [Full Text] [PDF]

				M. Stefan, H. Ji, R. A. Simmons, D. E. Cummings, R. S. Ahima, M. I. Friedman, and R. D. Nicholls Hormonal and Metabolic Defects in a Prader-Willi Syndrome Mouse Model with Neonatal Failure to Thrive Endocrinology, October 1, 2005; 146(10): 4377 - 4385. [Abstract] [Full Text] [PDF]