| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
The studies were conducted with a mouse model close to the pathophysiology of type 2 diabetes, streptozotosin and nicotinamide treatment (STZ/NA) or NSY mice and the in vitro systems to clarify a possible prevention of insulin resistance by internal redox control and its mechanisms. Although the glucose tolerance ability was suppressed by zinc deficiency as well as selenium deficiency of STZ/NA mice, the supplemented zinc was not likely to improve the insulin resistance.
As there was a possibility that insulin resistance might be caused by highly supplemented selenium, the relevance to the metabolisms of thyroid hormone or selenoprotein expressions was investigated. The results suggested that the expressions of glutathione peroxidase 1 and selenoprotein P 1 were related to the pathogenesis of the insulin resistance of NSY mice.
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