Efeito do consumo de café sobre o remodelamento do tecido adiposo em modelo murinho de obesidade

• Ano de defesa: 2021
• Autor(a) principal: Martins, Bruna Cadete
• Outros Autores: [e-mail]
• Orientador(a): Daleprane, Julio Beltrame
• Banca de defesa: Arruda, Sandra Fernandes , Mello, Vanessa de Souza
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade do Estado do Rio de Janeiro
• Programa de Pós-Graduação: Programa de Pós-Graduação em Alimentação, Nutrição e Saúde
• Departamento: Centro Biomédico::Instituto de Nutrição
• País: Brasil
• Palavras-chave em Português: Obesidade; Tecido adiposo; Inflamação; Browning; Termogênese adaptativa; Café
• Palavras-chave em Inglês: Obesity; Adipose tissue; Inflammation; Browning; Adaptive thermogenesis; Coffee
• Área do conhecimento CNPq: CIENCIAS DA SAUDE::NUTRICAO
• Link de acesso: http://www.bdtd.uerj.br/handle/1/19502

Obesity is a global public health problem, of multifactorial origin, with negative repercussions on health, with an increase in adipose tissue mass. Adipose tissue is composed of different cells, including adipocytes. Adipocytes can be white, characterized as an energy reservoir, or brown adipocytes, specialized in energy production, dissipating it in the form of heat, thus increasing energy expenditure. Additionally, adipocytes classified as beige, which are TAB adipocytes that express thermogenic genes similar to TAM, characterizing the effect known as browning. Recent studies demonstrate that transdifferentiation from TAB to TAM can be mediated by bioactive compounds present in food. Coffee is a popular food, rich in bioactive compounds that have biological effects resulting from the synergistic action of these compounds. The objective of this work was to evaluate the preventive and therapeutic effect of coffee consumption on the metabolic and molecular aspects of adipose tissue remodeling in a murine model of high-fat diet-induced obesity. Fifty 90-day-old C57BL/6 mice were divided into three groups: Control (C) standard diet AIN-93M (n=10); High-fat (HF) high-fat diet lard-rich diet with 50% energy from lipids (n=25) and Prevention Coffee (HF-CP) lard-rich diet with 50% energy from added lipids 1% w/w coffee (n=15). After 10 weeks, the HF group gave rise to the treatment coffee group (HF-CT) a lard-rich diet with 50% energy from lipids added with 1% w/w coffee (n=15). At the end of the experiment, the HF-CP group had lower body mass than the HF group (-8%, p<0.05) and better distribution of TA, with greater mass for the subcutaneous TAB compartment, TAM and reduced TAB visceral. In addition, the adipocytes from the epididymal TAM of the HF-CP group showed less hypertrophy and a smaller mean sectional area. In the HF-CT group, this improvement was slighter. Both groups that received coffee associated with a high-fat diet showed an improvement in glucose metabolism when compared to the HF group, and the glucose tolerance test in the HF-CP group was similar to that in the C group, and although the HF-CT group, did not equal the same value as in group C, it was lower than in group HF (-8%, p<0.05). Coffee consumption prevented hyperinsulinemia and hyperleptinemia in the HF-CP group and in the HF-CT group only hyperinsulinemia. The plasma concentration of IL-6 was reduced in the groups treated with coffee when compared to the HF group. The expression of genes involved in adaptive thermogenesis and mitochondrial biogenesis was higher in the TAB and TAM of HF-CP and HF-CT animals, being the most effective prevention model, as well as the immunofluorescence of UCP-1 in the TAM of these animals. Coffee showed better effects when consumed preventively with better TA remodeling, with the maintenance of the brown phenotype, thermogenic activity. Furthermore, it was able to attenuate body mass gain, improve glucose and leptin homeostasis. When consumed after obesity induction, as a treatment, there was also better AT remodeling with attenuation of whitening, greater expression of thermogenic genes and reversal of hyperinsulinemia.