Efeitos do extrato de Euterpe oleracea Mart. (Açaí) na esteatose hepática associada a obesidade: papel do sistema renina-angiotensina

• Autor(a) principal: Romão, Matheus Henrique
• Data de Publicação: 2019
• 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/1/12723
• topic: Obesity; Hepatic steatosis; Poliphenols; Renin-angiotensin system; Obesidade; Esteatose hepática; Polifenóis; Sistema renina-angiotensina; Obesidade; Açaí Uso terapêutico; Sistema renina-angiotensina; Esteatose hepática; Polifenóis; CNPQ::CIENCIAS BIOLOGICAS::FARMACOLOGIA::FARMACOLOGIA CLINICA

Obesity is associated with the development of several metabolic alterations, such as hypertension. The elevation of the renin angiotensin system (RAS) observed in obesity is related to the development of insulin resistance, which can lead to hepatic steatosis, which is the accumulation of fat in the liver. Previous studies have demonstrated that the hydroalcoholic extract of the açaí stone (ASE) acts in an experimental model of obesity, preventing hypertension, dyslipidemia, weight gain and hyperglycemia. In addition to these effects, ASE demonstrated in the renovascular hypertension model the ability to modulate RAS components, reducing plasma renin levels. The aim of this study was to evaluate the preventive effect of ASE treatment on hepatic alterations in an obesity animal model, comparing it with the effects of RAS inhibitors: enalapril (ENA) and telmisartan (TEL). 30 day old male C57BL / 6 mice were separated into five control groups (diet 10% lipids); HF (60% lipid diet); HF + ASE (300 mg / kg-1), HF + ENA (30 mg / kg-1) and HF + TEL (10 mg / kg-1). The diet was administered concomitantly with these treatments, which were performed by intragastric gavage for 12 weeks. Body mass and glycemia were evaluated during the treatment period. At the end of treatment and after euthanasia, liver weight, visceral adipose tissue weight, Lee index, caloric intake, liver lipid profile, antioxidant enzyme activity and oxidative damage in liver homogenate were evaluated. In addition, the protein expression of the components of the RAS and factor NF-kB was evaluated by western blotting in liver homogenate. Hepatic steatosis was evaluated histologically. In the HF group there was an increase in body weight and blood glucose, changes that were prevented by the treatment with ASE and ENA. The HF group also showed an increase in visceral adipose tissue weight, caloric intake and Lee's index. Treatment with ASE prevented the increase of adipose tissue weight and Lee's index, treatment with ENA prevented all these increases and the TEL was not able to prevent these changes. All treatments prevented the increase of hepatic levels of cholesterol and triglycerides observed in the HF group. Increased liver weight and steatosis were prevented by ASE and ENA treatments. All treatments prevented the reduction of the antioxidant activity observed in the HF group. The HF group showed increased expression of renin and AT1. All treatments decreased renin expression, only treatment with TEL decreased AT1 expression. Treatment with ASE increased the expression of ECA-2 and Mas. These results indicate that the ASE prevented the deleterious effects of the HF diet on the liver and could be effective compared to the ENA. The beneficial effects of ASE involve the reduction of weight gain, the antioxidant effect and also the modulation of RAS, proving to be an important tool in the treatment of hepatic steatosis