RESUMO
The Diabetes Mellitus (DM) is a chronic disease associated with loss of brain regions such as the cerebellum, increasing the risk of developing neurodegenerative diseases such as Parkinson's disease (PD). In the brain of diabetic and PD organisms the insulin/IGF-1 signaling is altered. Exercise training is an effective intervention for the prevention of neurodegerative diseases since it release neurotrophic factors and regulating insulin/IGF-1 signaling in the brain. This study aimed to evaluate the proteins involved in the insulin/IGF-1 pathway in the cerebellum of diabetic rats subjected to exercise training protocol. Wistar rats were distributed in four groups: sedentary control (SC), trained control (TC), sedentary diabetic (SD) and trained diabetic (TD). Diabetes was induced by Alloxan (ALX) (32mg/kgb.w.). The training program consisted in swimming 5days/week, 1h/day, during 6 weeks, supporting an overload corresponding to 90% of the anaerobic threshold. At the end, cerebellum was extracted to determinate the protein expression of GSK-3ß, IRß and IGF-1R and the phosphorylation of ß-amyloid, Tau, ERK1+ERK2 by Western Blot analysis. All dependent variables were analyzed by one-way analysis of variance with significance level of 5%. Diabetes causes hyperglycemia in both diabetic groups; however, in TD, there was a reduction in hyperglycemia compared to SD. Diabetes increased Tau and ß-amyloid phosphorylation in both SD and TD groups. Furthermore, aerobic exercise increased ERK1+ERK2 expression in TC. The data showed that in cerebellum of diabetic rats induced by alloxan there are some proteins expression like Parkinson cerebellum increased, and the exercise training was not able to modulate the expression of these proteins.
Assuntos
Cerebelo/metabolismo , Diabetes Mellitus Experimental/metabolismo , Hiperglicemia/metabolismo , Fator de Crescimento Insulin-Like I/metabolismo , Transdução de Sinais , Animais , Glicemia/metabolismo , Diabetes Mellitus Experimental/fisiopatologia , Masculino , Tecido Nervoso/metabolismo , Condicionamento Físico Animal , Ratos Wistar , Transdução de Sinais/fisiologiaRESUMO
Diabetes mellitus is a chronic disease that has been associated with memory loss, neurological disorders, and Alzheimer's disease. Some studies show the importance of physical exercise to prevent and minimize various neurological disorders. It is believed that the positive effects of exercise on brain functions are mediated by brain insulin and insulin-like growth factor-1 (IGF-1) signaling. In this study, we investigate the role of swimming exercise training on hippocampus proteins related to insulin/IGF-1 signaling pathway in Type 1 diabetic rats and its effects on spatial memory. Wistar rats were divided into four groups namely sedentary control, trained control, sedentary diabetic (SD), and trained diabetic (TD). Diabetes was induced by Alloxan (ALX) (32 mg/kg b.w.). The training program consisted in swimming 5 days/week, 1 h/day, per 6 weeks, supporting an overload corresponding to 90% of the anaerobic threshold. We employed ALX-induced diabetic rats to explore learning and memory abilities using Morris water maze test. At the end of the training period, the rats were sacrificed 48 h after their last exercise bout when blood samples were collected for serum glucose, insulin, and IGF-1 determinations. Hippocampus was extracted to determinate protein expression (IR, IGF-1R, and APP) and phosphorylation (AKT-1, AKT-2, Tau, and ß-amyloide proteins) by Western Blot analysis. All dependent variables were analyzed by two-way analysis of variance with significance level of 5%. Diabetes resulted in hyperglycemia and hypoinsulinemia in both SD and TD groups (P < 0.05); however, in the training-induced group, there was a reduction in blood glucose in TD. The average frequency in finding the platform decreased in SD rats; however, exercise training improved this parameter in TD rats. Aerobic exercise decreased Tau phosphorylation and APP expression, and increased some proteins related to insulin/IGF-1 pathway in hippocampus of diabetic rats. Thus, these molecular adaptations from exercise training might contribute to improved spatial learning and memory in diabetic organisms.
Assuntos
Diabetes Mellitus Experimental/fisiopatologia , Fator de Crescimento Insulin-Like I/metabolismo , Insulina/sangue , Condicionamento Físico Animal , Memória Espacial/fisiologia , Natação , Animais , Análise Química do Sangue , Glicemia , Western Blotting , Peso Corporal , Hipocampo/fisiopatologia , Hiperglicemia/fisiopatologia , Masculino , Aprendizagem em Labirinto/fisiologia , Atividade Motora , Distribuição Aleatória , Ratos Wistar , Análise e Desempenho de TarefasRESUMO
Este estudo foi delineado para desenvolver um modelo animal de hiperlipemia crônica, independente de manipulaçäo dietética, visando análise da interaçäo metabólica glicose/ácidos glaxos livres(AGL) no exercício. Ratos com 60 dias foram separados em 4 grupos e tratados por 6 semanas: Sedentário/Heparina - receberam diariamente uma aplicaçäo de heparina (250 U/kg), para elevar os AGL circulantes; Sedentário/Salina - receberam diariamente uma aplicaçäo de salina(NaCI 0,9 porcento); Treinado/Heparina - receberam heparina e foram submetidos à nataçäo, 1h/dia, 5 dias/semana, com sobrecarga de 5 porcento p.c. e Treinamento-Salina - receberam salina e foram submetidos à nataçäo. Os animais "heparina" apresentaram AGL séricos elevados durante parte do dia. Glicose e insulina basais no soro e insulina no pâncreas foram semelhantes para todos os grupos. Glicogênio do músculo sóleo foi maior nos treinados que nos sedentários. Durante teste de tolerância à glicose os animais "heparina" apresentaram área sob a curva de insulina superior e área sob a curva de glicose semelhantes às dos "salina". A presenta de AGL näo afetou a depleçäo do glicogênio do músculo sóleo isolado em nenhum grupo. Em resumo, os efeitos crônicos da elevaçäo da disponibilidade de AGL alteraram a utilizaçäo periférica de glicose enquanto que o aumento agudo näo o fez. O modelo parece viável para estudos da interaçäo metabólica glicose/AGL no exercício.(au)