Efeito da obesidade sobre parâmetros inflamatórios e bioquímicos no hipotálamo de camundongos

• Ano de defesa: 2016
• Autor(a) principal: Schraiber, Rosiane de Bona
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Hipotálamo; Obesidade; Estresse oxidativo; Metabolismo
• Link de acesso: https://repositorio.animaeducacao.com.br/handle/ANIMA/3069

Introduction: Obesity is a chronic disease whose pathophysiology involves changes in peripheral tissues and in the central nervous system (CNS). In this context, many researchers seek to understand the influence of saturated fat intake on the hypothalamus, a key structure in the food control. Objective: Assess inflammatory parameters of oxidative stress and energy metabolism in the hypothalamus of mice led to an animal model of obesity. Methodology: Swiss mice were divided into two study groups: control group and obese group. The control animals were fed with a diet with adequate amounts of macronutrients (standard diet), while the animals in the obese group were induced to obesity through the consumption of a diet high in saturated fat (high fat diet). Obesity induction had a duration of 10 weeks, and at the end of this period, the disease model was validated in animals. Shortly thereafter, the mice were euthanized; tissues of interest were dissected and taken for biochemical analysis. Results: Animals in the obese group had higher calorie consumption and, allied to this, had higher body weight and higher weight of mesenteric fat, compared to the control group. Obesity presented an increase in the levels of interleukin 1β (IL-1β) and decreased levels of interleukin 10 (IL-10) in the hypothalamus of animals. In addition, there was increased lipid peroxidation and protein carbonylation, coupled with the lower level of GSH in the hypothalamus of obese animals. However, there was no statistically significant difference in the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in the hypothalamus of both groups. The obese group had lower activity of complex I, II and IV of the mitochondrial respiratory chain, as well as lower activity of creatine kinase (CK) in the hypothalamus. Conclusion: Obesity presented inflammation, oxidative stress and mitochondrial dysfunction in the hypothalamus, a key structure in the food control.