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Submitted on September 30, 2005
Accepted on February 16, 2006
Department of Pediatrics (K.H.P, Y.H.C., E.K.K., W.Y.S., D.-K.J.), Department of Orthopedic Sports Medicine (W.H.P), Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul; Clinical Research Center (Y.J.O., A.H.K., S.H.C, S.W.K., S.J.H), Samsung Biomedical Research Institute, Seoul, Korea
* To whom correspondence should be addressed. E-mail: jindk{at}smc.samsung.co.kr.
Context: Decreased fasting ghrelin levels and decreased ghrelin suppression in overweight children have been reported to be associated with insulin resistance. However, Prader-Willi syndrome (PWS) is associated with increased total ghrelin levels and relative hypo-insulinemia.
Objective: To analyze changes in acylated ghrelin (AG) and des-acylated ghrelin (DAG) levels post glucose loading and to characterize correlations between insulin sensitivity and ghrelin suppression
Design: Plasma glucose, insulin, AG, and DAG levels were measured in PWS children (n = 11) and in normal obese controls (n = 10) during oral glucose tolerance testing (OGTT).
Setting: All subjects were admitted to the Samsung Medical Center.
Interventions: OGTT was performed in all subjects after an overnight fast.
Main Outcome Measures: Plasma levels of each of the following hormones were measured; AG, DAG, insulin, and those of glucose at 0, 30, 60, 90, and 120 min post glucose challenge and WBISI (whole body insulin sensitivity index) values were calculated .
Results: AG levels fell markedly more from fasting levels in PWS children than in normal healthy obese controls at 30, 60, and 90min post glucose challenge, but no significant differences in DAG levels were observed at any time between PWS patients and controls. Fasting AG and DAG levels were found to correlate with WBISI in PWS, and absolute suppressions (
from baseline) in AG at 30min post glucose challenge (nadir) were also correlated with WBISI in PWS (r=0.64, P = 0.035).
Conclusions: Our results suggest that AG is sensitively suppressed by insulin and that this suppression correlated with insulin sensitivity in PWS children.
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