Estudo do metabolismo energético do tecido adiposo marrom em camundongos obesos hiperalimentados na lactação

• Autor(a) principal: Guedes, Roberta de Moura
• Data de Publicação: 2016
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UERJ
• Texto Completo: http://www.bdtd.uerj.br/handle/1/12792
• topic: Energy metabolism; Brown adipose tissue; Overnutrition; Mitochondria; Obesity; Metabolismo energético; Tecido adiposo marrom; Hiperalimentação; Mitocôndria; Obesidade; Obesidade; Metabolismo energético; Tecido adiposo marrom; Mitocôndria; Hiperfagia; CNPQ::CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA DE ORGAOS E SISTEMAS::FISIOLOGIA ENDOCRINA

Obesity is a disease that is growing alarmingly and the main cause is the energetic imbalance. According with WHO, in 2013, about 42 millions children had overweight or obesity. Studies demonstrates that nutricional changes in critical periods of life such as pregnancy and lactation generate impairs in the short and long-term. Obesity impairs several tissues, including the brown adipose tissue (BAT). BAT is known to dissipate energy as heat instead ATP. Increases in BAT activity increased spending energetic, therefore has been focused on action in obesity. The main of our work was to observe if young Swiss mice demonstrates changes on the energetic metabolism in the BAT. Were used Swiss mice at 21 days of life, overfed through reduction of litter size model. We evaluated blood s biometric and biochemists parameters; blood insulin; histology by hematoxylin and eosin; intraperitoneal glucose tolerance test (IGTT); protein content analyse by Western Blotting; high-resolution respirometry and ATP measurement. We observed increases in body weight; epididymal and retroperitoneal fat; plasmatic insulin; fasting glucose and plasma cholesterol and triglycerides in Overfeed Group (OG). Through histology, we noted whitening indicatives on BAT in GH. We saw in IGTT a higher in curve at 90 minutes. At WB we observed significant differences in GLUT1 content that is lower in GH; increases in ratio pAMPK/AMPK and decreases in PGC1α and SIRT1, favoring a decreases in mitochondrial biogenesis; decreases in FABP and PPARɣ content inducing impairs in fatty acids metabolism; increases in UCP1 content, showing a compensatory mechanism; decreases in adrenergic receptor β3 and hormone receptor thyroid content, impairing the adrenergic signaling; in relation to the electron transport system we observed decreases only complex 3 that is involved with angiogenesis in this tissue. In respirometry we observed decreases in oxidation using glutamate, malate and succinate in GH and decreases in ATP content in GH. Together, these data reinforces the hypothesis that overnutrition at early life lead impairs in energetic metabolism in brown adipose tissue in short-time lead obesity.