Molecular mechanisms on induction obesity and insulin resistance in detrained animals submitted a high-fat diet

• Autor(a) principal: Pauli, José Rodrigo
• Data de Publicação: 2007
• Outros Autores: Esper Cintra, Dennys, Rochete Ropelle, Eduardo, Teodoro de Souza, Cláudio, Contin Moraes, Juliana, Abdalla Saad, Mário José
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Motriz (Online)
• Texto Completo: https://www.periodicos.rc.biblioteca.unesp.br/index.php/motriz/article/view/814
• topic: Destreinamento. Obesidade. Resistência à insulina.

The termination of exercise training (detraining) results in rapid fat accretion, weight gain and insulin resistance in both humans and rats. There is evident relationship between physical inactivity and insulin resistance. Different mechanisms may be involved in insulin resistance in this animal model. The aim of this study was to investigate the PI3-kinase/Akt and CAP/Cbl signaling pathways both involved with insulin-stimulated glucose uptake in white adipose tissue in detrained and sedentary animals submitted a high-fat diet. Wistar rats were submitted to swimming training during 8 weeks. Next this period the animals stop the training and received a rich-fat diet. The proteins from the insulin signaling pathway were analyzed by immunoprecipitation and immunoblotting. The results demonstrated that detraining result in an increased body mass and rapid body fat accretion. This fact was associated with increases insulin responsiveness in adipose tissue through IRS/PI3-Kinase/Akt pathway in detrained rats fed with a rich-fat diet. In addition, the CAP/Cbl pathway in adipose tissue was more insulin responsives in the detrained animals feeding with a rich-fat diet than S-DHL animals. In conclusion, the cessation of exercise is accompanied by increased body mass and rapid fat accretion and this aspect to have relation at least in part to increased insulin responsiveness in adipose tissue through CAP/Cbl pathway.