Otro
Acute exercise decreases PTP-1B protein level and improves insulin signaling in the liver of old rats
Registro en:
Immunity and Ageing, v. 10, n. 1, 2013.
1742-4933
10.1186/1742-4933-10-8
WOS:000327218400001
2-s2.0-84874150350.pdf
2-s2.0-84874150350
Autor
de Moura, Leandro Pereira
Souza Pauli, Luciana Santos
Cintra, Dennys Esper
de Souza, Claudio Teodoro
da Silva, Adelino Sanchez Ramos
Marinho, Rodolfo
de Melo, Maria Alice Rostom
Ropelle, Eduardo Rochete
Pauli, José Rodrigo
Resumen
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 IRβ/PTP-1B and IRS-1/PTP-1B association in the liver when compared with young rats. Conversely, in the liver of exercised old rats, IRβ/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. © 2013 Moura et al; licensee BioMed Central Ltd.
Materias
Ítems relacionados
Mostrando ítems relacionados por Título, autor o materia.
-
Glucose-induced Insulin Secretion Is Impaired And Insulin-induced Phosphorylation Of The Insulin Receptor And Insulin Receptor Substrate-1 Are Increased In Protein-deficient Rats
Reis M.A.B.; Carneiro E.M.; Mello M.A.R.; Boschero A.C.; Saad M.J.A.; Velloso L.A. -
Glucose-induced insulin secretion is impaired and insulin-induced phosphorylation of the insulin receptor and insulin receptor substrate-1 are increased in protein-deficient rats
Reis, Marise A.B.; Carneiro, Everardo M.; Mello, Maria A.R.; Boschero, A. Carlos; Saad, Mario J. A.; Velloso, Licio A. -
Glucose-induced Insulin Secretion Is Impaired And Insulin-induced Phosphorylation Of The Insulin Receptor And Insulin Receptor Substrate-1 Are Increased In Protein-deficient Rats.
Reis, M A; Carneiro, E M; Mello, M A; Boschero, A C; Saad, M J; Velloso, L A