Development of specific substances evaluated by the regulation of glucose transporter involved in aging of brain

首先，我们试图阐明加速衰老易感菌株SAMP8的脑细胞能量代谢特征。我们发现，4- 8周龄的d -葡萄糖氧化速率，就在大脑出现缺陷之前，高于与年龄匹配的SAMR1和SAMR2，并且细胞表面膜中葡萄糖转运蛋白的增加与代谢增加有关。这两种增长在4- 8周龄和大脑皮层受到限制。接下来，我们考察了氧自由基与上述能量代谢变化的关系。我们发现，与SAMR1相比，SAMP8在4- 8周龄时仅在大脑皮层中脂质过氧化物和蛋白质羰基含量短暂增加。因此，在4 ~ 8周龄时，SAMP8脑细胞中过氧化氢的含量增加。比较两菌株大脑皮层过氧化物酶体中各种酶的活性。SAMP8过氧化氢酶活性降低，酰基辅酶a氧化酶活性升高。这些结果很可能为理解老年记忆损伤的启动机制提供一些线索，并有助于开发新的抗衰老药物。

First, we tried to clarify the characteristic of the energy metabolism in the brain cells of SAMP8, a substrain of accelerated senescence-prone strain. We found that the rate of D-glucose oxidation at 4- to 8-weeks of age, just before the appearance of deficits in the brain, was higher than that in age-matched SAMR1 and SAMR2 and that the increase in glucose transporter protein in the cell surface membrane was involved in the increased metabolism. Both the increases were restricted at 4- to 8-weeks of age and the cerebral cortex.Next, we examined the involvement of oxygen free radicals in relation to the above-mentioned change in the cnergy metabolism. We found the transient increase in the contents of lipid peroxides and protein carbonyl only in the cerebral cortex of SAMP8 at 4- to 8-weeks of age in comparison with SAMR1. Accordingly, the content of hydrogen peroxide was increased in the cerebral cells of SAMP8 at 4- to 8-weeks of age. In comparison of the various enzyme activities in the peroxisome in the cerebral cortex between the two strains. The decrease in the catalase activity and increase in acyl-CoA oxidase activity were observed in SAMP8.It is quite likely that these results provide some clues towards understanding the mechanism responsible for initiating the process of senile memory impairment in the brain and contribute the development of new therapeutic substances for aging.