RESUMO
It is now commonly accepted that chronic inflammation associated with obesity during aging induces insulin resistance in the liver. In the present study, we investigated whether the improvement in insulin sensitivity and insulin signaling, mediated by acute exercise, could be associated with modulation of protein-tyrosine phosphatase 1B (PTP-1B) in the liver of old rats. Aging rats were subjected to swimming for two 1.5-h long bouts, separated by a 45 min rest period. Sixteen hours after the exercise, the rats were sacrificed and proteins from the insulin signaling pathway were analyzed by immunoblotting. Our results show that the fat mass was increased in old rats. The reduction in glucose disappearance rate (Kitt) observed in aged rats was restored 16 h after exercise. Aging increased the content of PTP-1B and attenuated insulin signaling in the liver of rats, a phenomenon that was reversed by exercise. Aging rats also increased the IRß/PTP-1B and IRS-1/PTP-1B association in the liver when compared with young rats. Conversely, in the liver of exercised old rats, IRß/PTP-1B and IRS-1/PTP-1B association was markedly decreased. Moreover, in the hepatic tissue of old rats, the insulin signalling was decreased and PEPCK and G6Pase levels were increased when compared with young rats. Interestingly, 16 h after acute exercise, the PEPCK and G6Pase protein level were decreased in the old exercised group. These results provide new insights into the mechanisms by which exercise restores insulin signalling in liver during aging.
RESUMO
INTRODUÇÃO: Evidências apontam que a ingestão exacerbada de frutose pode desencadear distúrbios característicos da síndrome metabólica. OBJETIVOS: Analisar os efeitos da ingestão de dieta rica em frutose sobre aspectos metabólicos de ratos da linhagem Wistar. Adicionalmente, verificar a capacidade aeróbia através da identificação da máxima fase estável de lactato (MFEL). MÉTODOS: Dezesseis ratos foram separados em dois grupos de oito animais: a) controle, alimentados com dieta balanceada, e b) frutose, alimentados com dieta rica em frutose. Foram analisadas a tolerância à glicose (área sob a curva de glicose durante teste de tolerância à glicose), sensibilidade à insulina (taxa de remoção da glicose sérica após sobrecarga exógena de insulina), perfil lipídico sérico e concentração de lactato sanguíneo [lac]s durante exercício na intensidade da MFEL. RESULTADOS: Teste t não pareado (p < 0,05) revelou diferença para a tolerância à glicose e triglicérides, porém não houve diferença na sensibilidade à insulina e na [lac]s. Anova one way com post hoc de Newman-Keuls (p < 0,05) revelou diferença para a cinética da glicose durante o teste de tolerância, mas não para a cinética do lactato durante exercício na MSSL. CONCLUSÃO: As Alterações fisiológicas provocadas pela dieta rica em frutose e inerentes à síndrome metabólica não prejudicam a capacidade aeróbia de ratos.
INTRODUCTION: Evidence points that exacerbated ingestion of fructose may trigger disturbs characteristic of the metabolic syndrome. OBJECTIVES: To analyze the effects of a fructose rich diet on metabolic aspects of Wistar lineage rats. Additionally, to verify the aerobic capacity, through the identification of the maximal lactate steady state (MSSL). PROCEDURES: Sixteen rats were separated in two groups of eight animals: a) Control, fed a balanced diet, and b) fructose, fed a fructose-rich diet. The glucose tolerance, (area under serum glucose during a glucose tolerance test), insulin sensibility (glucose disappearance rate after exogenous insulin administration), serum lipid profile and blood lactate concentration [lac]b during exercise at MSSL intensity, have been analyzed. RESULTS: Non-paired t test (p<0.05) revealed difference between groups in the area under the curve of glucose and serum triglycerides, no difference in insulin sensibility or in [lac]b was detected, though. One-way ANOVA with Newman Keuls post hoc revealed difference in the glucose kinetics during tolerance test, but not in the lactate kinetics during the MSSL. CONCLUSION: The physiological alterations promoted by fructose-rich diet and intrinsic to the metabolic syndrome do not harm the aerobic capacity of rats.