RESUMO
BACKGROUND: Alloxan induces oxidative stress and hyperglycemia in animal models. Acatalasemic (catalase deficiency) mice are susceptible to alloxan-induced hyperglycemia. As the incidence of hyperglycemia induced by alloxan was reportedly improved when mice were fed a vitamin E supplemented diet, this protective effect was examined. METHODS: Acatalasemic and normal mice fed a vitamin E supplemented diet were treated with alloxan. The pancreas were examined with microscopy. We also isolated pancreatic islets of normal mice treated with alloxan. The glucose stimulated insulin secretion was examined. RESULTS: Vitamin E powerfully ameliorated the increase in apoptosis. Vitamin E increases insulin amounts secreted from pancreatic cells, but does not ameliorate the regulation of the glucose stimulated insulin secretion. CONCLUSIONS: It is suggested that the difference in the mice fed vitamin E supplemented diet is due to an increase of insulin secretion and that vitamin E supplementation may have a role in helping to slow the stages of diabetes mellitus.
Assuntos
Aloxano/toxicidade , Apoptose/efeitos dos fármacos , Hiperglicemia/prevenção & controle , Insulina/metabolismo , Pâncreas/metabolismo , Vitamina E/farmacologia , Acatalasia/genética , Acatalasia/metabolismo , Acatalasia/patologia , Animais , Apoptose/genética , Hiperglicemia/induzido quimicamente , Hiperglicemia/metabolismo , Hiperglicemia/patologia , Insulina/genética , Masculino , Camundongos , Pâncreas/patologiaRESUMO
OBJECTIVES: Alloxan generates hydrogen peroxide in the body, and a small amount of alloxan administered to acatalasemic mice results in diabetes. D-α-Tocopherol (vitamin E) is an antioxidant which helps prevent excess oxidation in the body. In this study, we examined the effect of vitamin E on diabetes caused by alloxan administration in mice. METHODS: Mice were maintained on a vitamin E-deprived diet and supplemented diet, respectively, for 14 weeks. Alloxan was then intraperitoneally administered, and blood glucose, glucose tolerance and the insulin level in mouse blood were examined. RESULTS: Hyperglycemia was observed in the mice maintained on the vitamin E-deprived diet. The incidence of hyperglycemia in the mice maintained on the vitamin E-deprived diet was significantly higher than that in the mice maintained on the supplemented diet. The abnormal glucose metabolism caused by alloxan administration was ameliorated by the vitamin E-supplemented diet. CONCLUSIONS: It is deduced that vitamin E can prevent a decrease of insulin concentration in the blood in this mouse model.