title: Characterization of fat distribution in Prader-Willi syndrome: relationships with adipocytokines and influence of growth hormone treatment.
abstract: Marked anthropometric changes are seen in Prader-Willi syndrome (PWS). Emaciation is observed during infancy, whereas severe obesity is found in older children and adults. Growth hormone (GH) treatment modifies the anthropometric changes in PWS patients. In this study, we examined changes in the body composition of 51 PWS patients (age range, 6-54 years; median, 16.5 years), with a focus on the amount of abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), VAT/SAT ratio, and serum levels of adipocytokines (adiponectin, leptin, and resistin). The relationships between VAT, SAT, and adipocytokines, and lipid abnormalities and type 2 diabetes in 24 patients with obese PWS were also evaluated. With increasing age, SAT and VAT both increased markedly, but in 18 patients receiving GH treatment, VAT remained low at ≤30 cm(2) . In the GH-completed patients (n = 19), VAT and SAT increased with age to levels similar to those in non-GH-treated patients (n = 14). In the obese group, adiponectin decreased as VAT increased (r = -0.35, P = 0.11). Leptin (r = 0.67, P < 0.001) and resistin (r = 0.45, P = 0.04) showed positive correlations with SAT. Total cholesterol, low-density lipoprotein, and triglyceride levels correlated negatively with adiponectin (r = -0.59, r = -0.56, r = -0.56, respectively, P < 0.05) and hemoglobin A1c (r = -0.42, P = 0.08). To maintain lower VAT and prevent cardiovascular disease risk factors, GH treatment may be advisable even in adult patients with PWS.
authors.affiliation: Department of Pediatrics, Dokkyo Medical University Koshigaya Hospital, Saitama, Japan. yuriko@amy.hi-ho.ne.jp
authors.forename: Yuriko
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Abe
authors.forename: Yuji
authors.initials: Y
authors.lastname: Oto
authors.forename: Hisashi
authors.initials: H
authors.lastname: Itabashi
authors.forename: Masahisa
authors.initials: M
authors.lastname: Shiraishi
authors.forename: Atsunori
authors.initials: A
authors.lastname: Yoshino
authors.forename: Kazuo
authors.initials: K
authors.lastname: Obata
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Murakami
authors.forename: Toshiro
authors.initials: T
authors.lastname: Nagai
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000293:Adolescent; D000328:Adult; D000886:Anthropometry; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects / Q000378:metabolism; D050218:Body Fat Distribution; D002648:Child; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology; D005260:Female; D006442:Glycated Hemoglobin / Q000235:genetics / Q000378:metabolism; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D050152:Intra-Abdominal Fat / Q000378:metabolism; D020738:Leptin / Q000097:blood*; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D008659:Metabolic Diseases / Q000097:blood / Q000503:physiopathology; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000503:physiopathology; D011218:Prader-Willi Syndrome / Q000188:drug therapy* / Q000235:genetics* / Q000503:physiopathology; D052243:Resistin / Q000097:blood*; D012189:Retrospective Studies; D050151:Subcutaneous Fat / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D055815:Young Adult
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D002784:Cholesterol; D006442:Glycated Hemoglobin; D019382:Human Growth Hormone; D020738:Leptin; D052243:Resistin; D014280:Triglycerides; C517652:hemoglobin A1c protein, human