Modulação da adipogênese pelo extrato do caroço de açaí em adipócitos 3T3-L1

• Autor(a) principal: Trindade, Patricia Leticia
• Data de Publicação: 2017
• 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/1/17261
• topic: Phenolic Compounds; Adipogenesis; Obesity; Nutrição; Açaí; Obesidade; Compostos fenólicos; Adipogênese; 3T3-L1; CIENCIAS DA SAUDE::NUTRICAO

Body adiposity is an important risk factor for the development of chronic non-communicable diseases (NCD). Studies on the process of adipogenesis have been extensively performed in in vitro models, to describe the molecular and cellular bases of adipose tissue development, thus allowing the formulation of therapeutic and preventive strategies of obesity. The açai seed extract (ASE) has been evidenced as a potential regulator of body mass, acting in reduction of the content of adipose tissue in experimental models of obesity. In this way, the aim of this study was to evaluate the effects of ASE on the modulation of adipogenesis. To perform the work, 3T3-L1 cells were differentiated into adipocytes. The cells were incubated with different concentrations of ASE in the previous period (Pretreatment) to induce cell differentiation and after it (Treatment). Tests of viability, accumulation of intracellular triglycerides, expression of proteins involved in lipid metabolism and cell death were performed. The results showed that the ASE exposure, in a dose dependent manner, led to a decrease (P<0.05) in proliferation and cell viability, inhibited (P<0.05) differentiation through the decreasing expression of transcription factors and adipogenic proteins (PPARɣ, SREBP-1 and FAS), in addition to promoting increased expression of P53 protein and cause cell death mediated by apoptosis and necrosis. Taken together, the results show the performance of the phenolic compounds present in ASE and reinforce, although in in vitro assays, the potential of this extract as a possible modulation factor of adipogenesis.