Mecanismos envolvidos na restrição do crescimento intrauterino induzida pelo nado durante a gravidez

• Ano de defesa: 2016
• Autor(a) principal: Arakaki, Aline Midori [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Physical exercise; Swimming; Pregnancy; Placenta; Glycogenic cells; Exercício físico; Nado; Gravidez; Células glicogênicas
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=4695942; http://repositorio.unifesp.br/handle/11600/47564

Studies have shown that intrauterine growth restriction (IUGR), ie, low birth weight is one of the leading causes of perinatal death and neonatal morbidity. A previous study of our group showed that our swimming protocol during pregnancy caused IUGR and low birth weight. As IUGR is a consequence of possible fetal, placental and maternal changes, this project sought to evaluate the mechanisms responsible for intrauterine growth restriction caused by our protocol for swimming during pregnancy in mice. For this, we used female C56BL / 6 females of 2-3 months (INFAR). The training consisted of 1 hour of swimming daily, 5 times a week, during all gestation. Before the birth of the offspring the blood of the pregnant females was collected as well as the placenta of three fetuses of each female. Subsequently, we evaluated whether our swimming protocol during pregnancy altered some plasma cytokines such as IL-6, leptin, insulin, C-PEP and the hormone corticosterone, as well as expression of placental genes were analyzed, such as B1R, PIGF, Leptin, IL-6 and 11?HSD2. In addition, a morphophysiological analysis of the placenta was performed by counting CG on the junctional zone of the placenta. Results of this project showed that in the plasma of the exercised group, the concentration of IL-6 and corticosterone was higher. In addition, their placentas had lower gene expression of all analyzed genes and less amount of GC than in sedentary animals. As expected, the cytokine IL-6 was increased in the exercised group, since the exercise promotes the release of this cytokine by the muscles. Increased corticosterone means that exercise was stressful for the animals, which contributes to fetal IUGR. In addition, the reduction in the expression of the 11?HSD2 enzyme in the placenta of the exercised group means that the fetus is exposed to higher concentrations of maternal glucocorticoids, which also contributed to low birth weight (LBW). We have seen that in the placental junction of the same placenta there is a significant reduction of GC, which also contributes to LBW. We believe that our swimming protocol during pregnancy causes several changes in maternal plasma, the expression of placental genes and their morphophysiology, and these changes may explain why offspring exercised during pregnancy are born smaller