Expressão da Desiodase do Tipo III no cérebro de filhotes de ratas obesas

• Autor(a) principal: Teixeira, Cyntia Moraes
• Data de Publicação: 2012
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações do Mackenzie
• Texto Completo: http://dspace.mackenzie.br/handle/10899/22510
• topic: obesidade materna; desiodase; obesidade infantil; BDNF; hipotireoidismo; maternal obesity; deiodinase; childhood obesity; BDNF; hypothyroidism; CNPQ::CIENCIAS HUMANAS::PSICOLOGIA

Obesity has been considered epidemic in the whole world and is a risk factor for the development of hypertension, dyslipidemia, hyperglycemia, type 2 diabetes and hepatic steatosis. The increase of obesity in during pregnancy not only increases the risk of developing cardiovascular diseases but may also be related to abnormalities in the developing CNS of embryos, for example, reduction of potential long-term (LTP) in the hippocampus and neurogenesis . It is possible that the reduced levels of BDNF observed in these embryos, are involved with the injury in the processes of learning and memory observed in these animals. Studies also show that BDNF is reduced in fetuses of mothers with maternal subclinical hypothyroidism. These puppies have worsening neurological development, with deficits in long and short term memory. Here we evaluated whether maternal obesity may alter levels of BDNF and enzyme expression of type III deiodinase (D3) in the brains of pups, with consequent alteration of local levels of T3 to 7 °, 10 ° and 16 ° day-old post -natal. Our results showed that obesity reduced the expression of D3 on the 7th day of postnatal life of the offspring of obese mothers, but not in later days. There were no significant alterations in the levels of BDNF in any of the evaluated days. Our data suggest that it is possible that thyroid hormone is involved in neurophysiological abnormalities observed in offspring of obese rats.