Ghrelin levels in young children with Prader-Willi syndrome
Received 1 April 2005; received in revised form 11 January 2006; accepted 13 April 2006.
Objective
To explore the hypothesis that high ghrelin levels contribute to obesity in Prader-Willi syndrome (PWS), we assessed whether the increased levels observed in older persons with PWS exist in very young children, before the onset of hyperphagia.
Study design
We measured ghrelin levels in nine children with PWS (17-60 months of age) and eight healthy control subjects of equivalent body mass index (BMI), age, and sex.
Results
PWS and control groups had equivalent BMI (16.8 ± 1.4 vs 16.1 ± 0.9 kg/m2, respectively; P = .24), age (37.8 ± 15.4 vs 50.3 ± 17.7 months; P = .14), and sex. PWS and control groups also had equivalent fasting levels of total ghrelin (787 ± 242 vs 716 ± 135 pg/mL, respectively; P = .24), bioactive ghrelin (102 ± 35 vs 91 ± 23 pg/mL; P = .45), insulin, and glucose. Ghrelin correlated negatively with BMI among controls (r = −0.760, P = .029) but not PWS (r = 0.015, P = .97).
Conclusions
Children <5 years of age with PWS, who had not yet developed hyperphagia or excessive obesity, had normal ghrelin levels, in contrast with the hyperghrelinemia of older, hyperphagic people with PWS. It is possible that ghrelin levels increase suddenly before hyperphagia develops.
Department of Pediatrics, Division of Developmental and Behavioral Pediatrics, Madigan Army Medical Center, Fort Lewis; the Center of Human Development and Disability, Department of Pediatrics, University of Washington School of Medicine, Seattle; and the Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, VA Puget Sound Health Care System, Seattle, Washington.
Reprint requests: Dr David E. Cummings, Associate Professor of Medicine, University of Washington, VA Puget Sound Health Care System, 1660 South Columbian Way, S-111-Endo, Seattle, WA 98108.
Supported by NIH grants RO1 DK61516 and PO1 DK68384 (to D.E.C.).
ABSTRACT