Evidences of metabolic disruptor hypothesis: perinatal exposure to BPA impairs neuroendocrine mechanisms regulating food intake in adult male rats.

STOKER C; ANDREOLI MF; ROSSETTI MF; KASS L; BOSQUIAZZO VL; RAMOS JG

Congreso; 11° Reunión Bianual SETAC Latinoamérica; 2015

Obesity and metabolic syndrome are endocrine diseases and thus sensitive to environmental agents that can interfere with hormone and neuroendocrine action. Bisphenol A (BPA) is a compound used in the polymerization of polycarbonate plastics and is an endocrine disrupter (EDs). Kisspeptin (kiss1), a hypothalamic neuropeptide that drives fertility by stimulating GnRH secretion, has been proposed to be the link between energy balance and reproductive function. We previously demonstrate that BPA impairs glucose homeostasis and induces an increase in body weight as a consequence of a higher energy intake.Here, we evaluate the influence of perinatal exposure to a dose considered safe of BPA on hypothalamic signals that regulate food intake, both in adult males fed with control diet (CD) or a high fat diet (HFD).Male rats were exposed to 50 g/kg/day of BPA or vehicle (0.002 % ethanol) from day 9 of gestation to weaning in the drinking water. Since weaning, males were fed with CD or HFD for 20 weeks. We evaluated hypothalamic mRNA expression of the neuropeptides: Kiss1, POMC, CART, AGRP, NPY; the receptors: ER, ER and the relative activity of its promoters (OS, O, OT, and E1). In BPA exposed animals fed with CD, the higher energy intake was mediated by a down regulation of the neuropeptides CART, NPY, and the receptors ER ERand its promoters (p