title: Elevated fasting plasma ghrelin in prader-willi syndrome adults is not solely explained by their reduced visceral adiposity and insulin resistance.
abstract: Plasma ghrelin is elevated in Prader-Willi syndrome (PWS). This might contribute to obesity or GH deficiency in such patients. Visceral adiposity and insulin resistance are reduced in PWS, which might lead to hyperghrelinemia. We measured fasting plasma ghrelin in control female (n = 39), PWS female (n = 12), and PWS male (n = 6) adults. In controls and PWS, ghrelin was negatively correlated with visceral adiposity, fasting insulin, and homeostasis model insulin resistance index. There was no significant correlation with serum IGF-I in PWS. In stepwise linear regression, visceral adiposity (P < 0.02) had a stronger inverse correlation with ghrelin than sc fat depots in controls and PWS, possibly through hyperinsulinemia, as the correlations with insulin resistance were even stronger (P < 0.01). PWS females had significantly (P < 0.001) elevated ghrelin (mean +/- SD, 661 +/- 360 pg/ml), compared with both nonobese (363 +/- 163) and obese (191 +/- 66) controls. Ghrelin was increased 3.4- to 3.6-fold in PWS females adjusting for total adiposity, 3.2- to 3.4-fold adjusting for visceral adiposity, and 3.0-fold adjusting for insulin resistance. Fasting plasma glucagon-like peptide-1 was normal in PWS females. The hyperghrelinemia in PWS adults is therefore not solely explained by their reduced visceral adiposity and relative hypoinsulinemia. Its cause and consequences await further elucidation.
authors.affiliation: Department of Endocrinology, St. Bartholomew's Hospital, London, United Kingdom EC1A 7BE. tgoldstone@yahoo.com
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Goldstone
authors.forename: E Louise
authors.initials: EL
authors.lastname: Thomas
authors.forename: Audrey E
authors.initials: AE
authors.lastname: Brynes
authors.forename: Gabriela
authors.initials: G
authors.lastname: Castroman
authors.forename: Ray
authors.initials: R
authors.lastname: Edwards
authors.forename: Mohammad A
authors.initials: MA
authors.lastname: Ghatei
authors.forename: Gary
authors.initials: G
authors.lastname: Frost
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Holland
authors.forename: Ashley B
authors.initials: AB
authors.lastname: Grossman
authors.forename: Márta
authors.initials: M
authors.lastname: Korbonits
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Bloom
authors.forename: Jimmy D
authors.initials: JD
authors.lastname: Bell
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D016022:Case-Control Studies; D005215:Fasting / Q000097:blood*; D005260:Female; D054439:Ghrelin; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D036361:Peptide Hormones / Q000097:blood*; D011218:Prader-Willi Syndrome / Q000097:blood / Q000473:pathology* / Q000503:physiopathology*; D011498:Protein Precursors / Q000097:blood; D012044:Regression Analysis; D014781:Viscera
chemical_list: D054439:Ghrelin; D010446:Peptide Fragments; D036361:Peptide Hormones; D011498:Protein Precursors; D052216:Glucagon-Like Peptide 1; D005934:Glucagon