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PWSA (USA) Research Grant Approved Oct. 2000/Aug. 2001…Published Results
J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):260-2.
“Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI”
(Shapira NA, Lessig MC, He AG, James GA, Driscoll DJ, Liu Y.)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15654046&query_hl=1&itool=pubmed_docsum 

The neurobiology relating to the insatiable appetite observed in Prader-Willi syndrome (PWS) has not been fully characterized. 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.

edited: 02/09/2012

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