title: In adults with Prader-Willi syndrome, elevated ghrelin levels are more consistent with hyperphagia than high PYY and GLP-1 levels.
abstract: OBJECTIVE
  Prader-Willi syndrome (PWS) is a leading genetic cause of obesity, characterized by hyperphagia, endocrine and developmental disorders. It is suggested that the intense hyperphagia could stem, in part, from impaired gut hormone signaling. Previous studies produced conflicting results, being confounded by differences in body composition between PWS and control subjects.
  
  
  METHODS
  Fasting and postprandial gut hormone responses were investigated in a cross-sectional cohort study including 10 adult PWS, 12 obese subjects matched for percentage body fat and central abdominal fat, and 10 healthy normal weight subjects.
  
  
  METHODS
  PYY[total], PYY[3-36], GLP-1[active] and ghrelin[total] were measured by ELISA or radioimmunoassay. Body composition was assessed by dual energy X-ray absorptiometry. Visual analog scales were used to assess hunger and satiety.
  
  
  RESULTS
  In contrast to lean subjects (p<0.05), PWS and obese subjects were similarly insulin resistant and had similar insulin levels. Ghrelin[total] levels were significantly higher in PWS compared to obese subjects before and during the meal (p<0.05). PYY[3-36] meal responses were higher in PWS than in lean subjects (p=0.01), but not significantly different to obese (p=0.08), with an additional non-significant trend in PYY[total] levels. There were no significant differences in self-reported satiety between groups, however PWS subjects reported more hunger throughout (p=0.003), and exhibited a markedly reduced meal-induced suppression of hunger (p=0.01) compared to lean or obese subjects.
  
  
  CONCLUSIONS
  Compared to adiposity-matched control subjects, hyperphagia in PWS is not related to a lower postprandial GLP-1 or PYY response. Elevated ghrelin levels in PWS are consistent with increased hunger and are unrelated to insulin levels.
authors: Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Sydney-Darlinghurst, Australia. l.purtell@garvan.org.au
authors: Louise
authors: L
authors: Purtell
authors: Lisa
authors: L
authors: Sze
authors: Georgina
authors: G
authors: Loughnan
authors: Ellie
authors: E
authors: Smith
authors: Herbert
authors: H
authors: Herzog
authors: Amanda
authors: A
authors: Sainsbury
authors: Katharine
authors: K
authors: Steinbeck
authors: Lesley V
authors: LV
authors: Campbell
authors: Alexander
authors: A
authors: Viardot
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005215:Fasting; D005260:Female; D054439:Ghrelin / Q000097:blood*; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D006801:Humans; D006815:Hunger; D006963:Hyperphagia / Q000097:blood* / Q000209:etiology; D007328:Insulin / Q000097:blood; D008297:Male; D009765:Obesity / Q000209:etiology; D019894:Peptide YY / Q000097:blood*; D019518:Postprandial Period; D011218:Prader-Willi Syndrome / Q000097:blood* / Q000150:complications; D015398:Signal Transduction / Q000502:physiology; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D054439:Ghrelin; D007328:Insulin; D019894:Peptide YY; D052216:Glucagon-Like Peptide 1