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Fasting Ghrelin Levels Are Not Elevated in Children with Hypothalamic Obesity

Department of Paediatrics (S.K.), Royal Alexandra Hospital, Brighton BN1 3JN, United Kingdom; Department of Complex Biochemistry (R.G.), Department of Endocrinology and Diabetes (C.C.P., G.L.W., M.R.Z.), and Clinical Epidemiology and Biostatistics Unit (S.D.), Murdoch Children’s Research Institute, The Royal Children’s Hospital, Melbourne 3052, Australia; and Department of Endocrinology (M.H.), Mater Children’s Hospital, Brisbane 4101, Australia

Address all correspondence and requests for reprints to: Dr. Mark Harris, Mater Children’s Hospital, Raymond Terrace, South Brisbane, 4101, Queensland, Australia. E-mail: mark.harris{at}mater.org.au.

Morbid obesity is a common problem after damage to the hypothalamus. Hypothalamic dysfunction is also thought to underlie the obesity that is typical of Prader-Willi syndrome. Elevated fasting levels of the appetite-stimulating hormone ghrelin have been reported in Prader-Willi syndrome. The aim of this study was to determine whether fasting ghrelin levels are increased in children with hypothalamic obesity.

Fasting total ghrelin levels were compared in three groups: normal-weight controls (n = 16), obese controls (n = 16), and patients with hypothalamic obesity (n = 16). Obese children had lower fasting total ghrelin levels than normal controls, but there was no difference between the fasting total ghrelin level in obese controls and children with hypothalamic obesity (P = 0.88). These data suggest that it is unlikely that an elevation in fasting total ghrelin is responsible for the obesity that occurs after hypothalamic damage. Therapeutic interventions aimed at reducing fasting total ghrelin may prove ineffective in controlling weight gain in this group.