Abstract
Ghrelin, released from the stomach, acts at the hypothalamus and is associated with initiation of food intake. We hypothesised that patients with craniopharyngioma and hypothalamic obesity (CRHO) would have ghrelin abnormalities. Fifteen CRHO patients and 15 BMI-matched controls underwent oral glucose tolerance test with dynamic ghrelin measurement. From 0–30 minutes, ghrelin (pg/ml) decreased less (43.4 ± 38.8 vs. 70.8 ± 35.8, p < 0.05) and insulin (pmol/l) increased more (1 669.2 ± 861.7 vs. 1 049.1 ± 560.4, p = 0.04) in CRHO compared with controls, respectively. Insulin area-under-the-curve was a weak negative predictor of the 0–30 minutes ghrelin decrease (r2 = 0.29, p = 0.02). Delayed ghrelin suppression may contribute to obesity in CRHO.
Acknowledgements
The authors would like to acknowledge the suggestions and contributions of Dr Denis Daneman, Division of Endocrinology, Department of Pediatrics, The Hospital for Sick Children.
Declaration of interest: The study was supported by a Hospital for Sick Children Research Institute Seed Grant. COG, PP, KA, and JH have nothing to disclose. JSR was supported by a fellowship from the Canadian Pediatric Endocrine Group. The authors have no disclosures and no conflicts of interest. The authors alone are responsible for the content and writing of the paper.