ECE2016 Guided Posters Paediatric Endocrinology & Development (10 abstracts)
1Department Medicina y Cirugía Animal, Universidad de Córdoba, Cordoba, Spain; 2Laboratorio de Nefrología. Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Madrid, Spain; 3Unidad de Investigación y Servicio de Nefrología (Red in Ren), Instituto Maimónides de Investigación Biomédica de Córdoba/Hospital Universitario Reina Sofia, Cordoba, Spain; 4Unidad de Lípidos y Aterosclerosis. IMIBIC/Hospital Universitario Reina Sofía, Cordoba, Spain.
A relationship between obesity, plasma leptin concentration and primary hyperparathyroidism has been previously reported. To test the hypothesis that leptin directly stimulates parathyroid hormone (PTH) secretion, in vivo and in vitro experiments were conducted. In the in vivo studies leptin (200 μg/kg, ip) was administered to lean and obese (mutants that do not express active leptin receptor) Zucker rats. The in vitro experiments were carried out by exposing rat parathyroid glands to increasing concentrations of leptin (0, 0.1, 0.25, 0.5, 1, 2 and 4 μg/ml). After leptin administration, PTH increased progressively in the lean but not in the obese rats reaching a maximum at 60 min (from 34.5±3.7 pg/ml to 113.9±23 pg/ml, P=0.01) and then returned to baseline by 180 min. Changes in PTH after leptin administration were not associated with changes in 1,25(OH)2-vitamin D, fibroblastic growth factor 23 (FGF23), calcium or phosphorus. Moreover, in vitro, a dose-dependent increase in PTH secretion that started at leptin=0.25 μg/ml and kept rising until reaching a zenith at leptin=2 μg/ml was identified. In conclusion, the results of the present study demonstrate a direct stimulatory effect of leptin on PTH secretion and suggest the existence of an endocrine axis between adipose tissue, where leptin is mainly produced, and the parathyroid glands.