Exercise training in the aerobic/anaerobic metabolic transition prevents glucose intolerance in alloxan-treated rats

نویسندگان

  • Clécia Soares de Alencar Mota
  • Carla Ribeiro
  • Gustavo Gomes de Araújo
  • Michel Barbosa de Araújo
  • Fúlvia de Barros Manchado-Gobatto
  • Fabrício Azevedo Voltarelli
  • Camila Aparecida Machado de Oliveira
  • Eliete Luciano
  • Maria Alice Rostom de Mello
چکیده

BACKGROUND Ninety percent of cases of diabetes are of the slowly evolving non-insulin-dependent type, or Type 2 diabetes. Lack of exercise is regarded as one of the main causes of this disorder. In this study we analyzed the effects of physical exercise on glucose homeostasis in adult rats with type 2 diabetes induced by a neonatal injection of alloxan. METHODS Female Wistar rats aged 6 days were injected with either 250 mg/kg of body weight of alloxan or citrate buffer 0.01 M (controls). After weaning, half of the animals in each group were subjected to physical training adjusted to meet the aerobic-anaerobic metabolic transition by swimming 1 h/day for 5 days a week with weight overloads. The necessary overload used was set and periodically readjusted for each rat through effort tests based on the maximal lactate steady state procedure. When aged 28, 60, 90, and 120 days, the rats underwent glucose tolerance tests (GTT) and their peripheral insulin sensitivity was evaluated using the HOMA index. RESULTS The area under the serum glucose curve obtained through GTT was always higher in alloxan-treated animals than in controls. A decrease in this area was observed in trained alloxan-treated rats at 90 and 120 days old compared with non-trained animals. At 90 days old the trained controls showed lower HOMA indices than the non-trained controls. CONCLUSION Neonatal administration of alloxan induced a persistent glucose intolerance in all injected rats, which was successfully counteracted by physical training in the aerobic/anaerobic metabolic transition.

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عنوان ژورنال:
  • BMC Endocrine Disorders

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2008