Cited by 130Regulation of Appetite and ObesityGenetic Syndromes and ImprintingEating Disorders and Behaviors

Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI

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Shapira, N A·2005·Journal of Neurology, Neurosurgery & Psychiatry

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.

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Crossref · 10.1136/jnnp.2004.039024

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  • Shapira et al. showed that in patients with PWS there was a temporal delay in response to glucose ingestion in the resting-state activity of a distributed network implicated in the regulation of hunger and satiation, namely the hypothalamus, insular cortex, ventral basal ganglia, and ventromedial prefrontal cortex.

    “Shapira and colleagues [682] showed that in patients with PWS that there was a temporal delay in response to glucose ingestion in the resting-state activity of a distributed network implicated in the regulation of hunger and satiation, namely the hypothalamus, insular cortex, ventral basal ganglia, and ventromedial prefrontal cortex.”

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Research works printed but not linked: 2

  1. Shapira NA, Lessig MC, Lewis MH, et al. Effects of topiramate in adults with Prader-Willi syndrome. Am J Ment Retard 2004;109:299-307.
  2. Xiong J, Gao J-H, Lancaster JL, et al. Clustered pixels for functional MRI activation studies in human brain. Hum Brain Mapp 1995;3:210-25.

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Authors
Shapira, N. A.
Affiliations
University of Florida (US)
Corresponding author
Shapira, N A
Venue
Journal of Neurology, Neurosurgery & Psychiatry
Publisher
BMJ
Published
2005-02-01
Volume
76
Issue
2
Pages
260-262
ISSN
0022-3050 (ISSN-L)
OpenAlex
W2124140144
Cited by
130
References
23
Citations by year
2026: 1 · 2025: 3 · 2024: 5 · 2023: 6 · 2022: 6 · 2021: 10 · 2019: 8 · 2018: 5 · 2017: 5 · 2016: 7 · 2015: 10 · 2014: 5 · 2013: 2 · 2012: 3
FWCI
3.06
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurology Neurosurgery & Psychiatry (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Florida Department of Health
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (R21NS045518, NS45518)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
Keywords
Prader-Willi syndrome, appetite, hypothalamus, glucose ingestion, topiramate, obesity, insula, ventromedial prefrontal cortex, nucleus accumbens
MeSH terms
Adult, Brain, Female, Humans, Magnetic Resonance Imaging, Male, Prader-Willi Syndrome, Satiety Response

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