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This version published online on January 30, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-2241
A more recent version of this article appeared on April 1, 2007
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Submitted on October 13, 2006
Accepted on January 22, 2007

Adiponectin levels in pre-pubertal children with Prader-Willi Syndrome before and during growth hormone therapy

D. A.M. Festen MD*, A. van Toorenenbergen PhD, H. J. Duivenvoorden PhD, and A.C.S. Hokken-Koelega MD, PhD

Dutch Growth Foundation, Rotterdam, The Netherlands; Department of Clinical Chemistry, NIHES, Department of Pediatric Endocrinology, Erasmus Medical Center Rotterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: d.festen{at}erasmusmc.nl.

Context: Children with Prader-Willi Syndrome (PWS) may have obesity and an abnormal body composition with a high body fat percentage, even if they have a normal body weight. Adiponectin has been inversely related to obesity and insulin resistance.

Objective: To evaluate in pre-pubertal PWS children (1) adiponectin levels, body composition, carbohydrate metabolism, and triglyceride levels, (2) associations between adiponectin and body composition, carbohydrate metabolism and triglycerides, and (3) effects of growth hormone (GH)-treatment on these outcome measures.

Patients: 20 pre-pubertal PWS children.

Intervention: The subjects were randomized into a GH-treatment group (n=10, 1mg/m2/day) and a non-GH treated control-group (n=10).

Main Outcome Measures: At baseline, after 1 and 2 years of GH-treatment, fasting levels of adiponectin, glucose, insulin, and triglycerides were assessed. Body composition and fat distribution were measured by Dual Energy X-ray Absorptiometry.

Results: PWS children had significantly higher median (interquartile range) adiponectin levels (17.1mg/l(13.9-23.2)) than healthy sex- and age-matched controls (11.8mg/l(9.7-12.5), p<0.005). Body fat percentage was significantly higher than 0 SDS (1.8 SDS(1.5-2.1), p<0.001). Adiponectin levels were inversely related to triglyceride levels (r=-0.52, p=0.03). There was a tendency to an inverse relation with body fat percentage and BMI, but no correlation with fasting insulin or glucose levels, the insulin/glucose ratio or HOMA-index. During GH-treatment, adiponectin levels increased significantly and did not change in randomized controls.

Conclusion: Adiponectin levels were increased, and inversely associated with triglyceride levels, in pre-pubertal, not overweight PWS children, although they had a relatively high body fat percentage. During GH-treatment, adiponectin levels further increased, whereas no change was found in the controls, which is reassuring with respect to the development of insulin resistance during GH-treatment.







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