Alterações cardiovasculares induzidas por supernutrição durante a lactação em ratos Wistar na idade adulta

• Ano de defesa: 2019
• Autor(a) principal: Ferreira Junior, Marcos Divino
• Orientador(a): Gomes, Rodrigo Mello
• Banca de defesa: Gomes, Rodrigo Mello, Mendes, Elizabeth Pereira, Matafome, Paulo Nuno Centeio
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Goiás
• Programa de Pós-Graduação: Programa de Pós-graduação em Ciências Biológicas (ICB)
• Departamento: Instituto de Ciências Biológicas - ICB (RG)
• País: Brasil
• Palavras-chave em Português: Obesidade; Sistema renina angiotensina; Hipertensão arterial; Hipertrofia ventricular
• Palavras-chave em Inglês: Disfunção endotelial obesity; Renin angiotensin system; Arterial hypertension; Ventricular hypertrophy; Endothelial dysfunction
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FARMACOLOGIA
• Link de acesso: http://repositorio.bc.ufg.br/tede/handle/tede/9539

Metabolic syndrome, closely related to obesity and its comorbidities, has become a worldwide pandemic, with increasing projections each year. The role of adipose tissue in the metabolic syndrome is not limited to the accumulation of lipids but also to the secretion of adipokines, which can control food consumption and energy expenditure. In obese individuals, there is a change in adipokines profile, from anti-inflammatory to pro-inflammatory. Inflammatory status in adipose tissue leads to insulin resistance, increased adipocyte differentiation and macrophages recruitment. In addition, the angiotensinogen (AGT) produced by adipose tissue may correspond to more than 30% of plasma levels of this substance, which increases in case of adipocyte hypertrophy. AGT is a key part of the Renin Angiotensin System (RAS), and is directly linked to circulating Angiotensin II (ANG II) levels, and the latter is linked to obesity-induced cardiovascular changes. Several studies have proposed to evaluate the effects of obesity on cardiovascular parameters, but the majority in animals with diet-induced obesity. Here, we aimed to evaluate the effects of postnatal overnutrition-induced obesity (PNO), due to litter reduction (SL), in metabolic and cardiovascular parameters in adulthood. In our study, SL group developed hyperphagia, greater adiposity and body weight, and dyslipidemia. Also, important cardiovascular alterations were developed in SL animals, such as hypertension, left ventricular hypertrophy, endothelial dysfunction, and increase of oxidative stress related proteins. However, through in vivo and ex vivo cardiac function analyzes, our results suggest that the hearts of animals in the SL group present neurohumoral compensation of their function, which leads to overload and may progress to heart failure. Taken together, our data may help in the elucidation of mechanisms by which obesity-induced cardiovascular changes occur, increasing the possibility of discovering new targets for treatment.