J Pharm Pharmacogn Res 2(Suppl. 1): S105, 2014
Special supplement with the abstract book of LATINFARMA 2013
C 035: EXPERIMENTAL HYPOTHYROIDISM DURING LACTATION ALTERS NEUROENERGETIC IN RAT CEREBELLUM
de Assis AM1, Müller AP1, Longoni A1, Farina M3, Perry MLS1,2, Souza DO.1,2
Thyroid hormone deficiency during perinatal development results in significant alterations in neurological functions. The relationship between such events and brain metabolism is not completely understood. The aim of this study was to investigate the effects of hypothyroidism on leucine, mannose, glucose, and lactate metabolism in rat cerebellar slices. Experimental hypothyroidism was induced by exposing mothers and pups to propylthiouracil (PTU) until weaning – postnatal day 21. Metabolic analyses were performed in postnatal day 10 (PND10) and 21 (PND21) animals. A matching group of animals received the same oral treatment also after weaning until adulthood postnatal day 60 (PND60) with T3 supplement during lactation (P1P21). In PND21 animals, PTU treatment significantly increased the rate of leucine oxidation to CO2, although glucose and lactate oxidations were not affected. PTU treatment also increased the oxidation of leucine to CO2 at PND60 (adult animals). PND10 hypothyroidism animals showed a decrease in conversion of mannose to glycolipids and glycoprotein compared to control group. However, PTU treatment increased the conversion of mannose to glycolipids and glycoprotein in PND21 animals. The replacement of T3 normalized mannose and leucine metabolism in adult rats. These results indicate that deficits in thyroid hormones during lactation could delay or alter brain development and metabolism.