| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2011: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2009: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2008: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Research Abstract |
It is becoming apparent that beta cell dysfunction observed in impaired insulin release is the essential element in the progression of diabetic patients. There are at least two populations of insulin secretory granules in beta cell, the RRP that is responsible for the initial(first phase) insulin release and a second reserve pool that is responsible for a more prolonged(second phase) insulin release. For now, it is still determined how these two types of insulin granules are involved in impaired insulin release In this study, we obtained the following results. 1) PDK1-Akt signaling pathway in beta cell mediated the potentiation of insulin release in the second phase. Akt signals seem to be involved in myosin Va-mediated actin network ; 2) Galpha o inactivation enhances insulin release. 3) CDKAL1, controls 1st phase insulin release.
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