| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Research Abstract |
We investigated mechanisms for apoptosis induction in pancreatic beta-cells, which can be responsible for impairment of insulin secretion in type 2 diabetes. The treatment of beta-cell line INS-1 with H_2O_2, which resembled diabetic oxidative stress, induced a transient intracellular Ca^<2+> elevation. The response was mediated by Ca^<2+> release from the endoplasmic reticulum through IP3 receptors and terminated within one hour. This seemed to become a trigger signal for beta-cell apoptosis induction ; the transient cytosolic Ca^<2+> elevation led to prolonged elevation of mitochondrial Ca^<2+> concentration, thereby inducing cytochrome c release from mitochondria and beta-cell apoptosis.
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