Estudo da hipertrofia cardíaca em animais knockout para o receptor adrenérgico Beta 3 no modelo de obesidade

Detalhes bibliográficos
Ano de defesa: 2019
Autor(a) principal: Brandão, Marllos Eduardo da Silva [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7654917
https://repositorio.unifesp.br/handle/11600/59804
Resumo: Obesity is the accumulation of body white adipose tissue and is positively related to systemic changes such as insulin resistance, hyperglycemia, hyperinsulinemia, dyslipidemia, hepatic steatosis and hypertension which together constitute the Metabolic Syndrome (MS). Left ventricular hypertrophy (LVH) is seen in the SM, which may aggravate cardiovascular complications and result in cardiac failure, sudden death and acute myocardial infarction. The hypothesis of our study contemplates the role of β3-adrenergic receptor (β3AR) as an important anti-hypertrophic agent, based on literature data suggesting that the β3-AR receptor has a negative inotropic effect on the heart and induces NO synthesis through of Oxyde Nitric Synthases (NOS) in cardiomyocytes and vessels. Specifically, we studied knockout mice for β3-AR (AR-β3KO) with MS induced by high-fat diet (40%) and evaluated changes in cardiac tissue through histological, immunohistochemical and protein expression analysis. HVE. Our results show that β3AR leads to concentric hypertrophy and left ventricular fibrosis, unlike FVB animals that developed eccentric hypertrophy. However, it was observed that LVH developed equally in the obese groups, showing that there was an independent β3AR mechanism.