| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Research Abstract |
It has been recognized that a paucity of β-cell mass is central in the pathogenesis of T2DM. Glycogen synthase kinase-3(Gsk-3) is negatively regulated by insulin receptor signaling. In this study, we aimed to understand role of Gsk-3β in the regulation of β-cell mass. β-cell specific ablation of Gsk-3β resulted in expanded β-cell mass and resistance to high fat feeding induced diabetes in mice. Furthermore, we have evidenced that Gsk-3 was implicated to an induction of apoptosis through a modulation of stress response in β-cells during ER stress. Taken together, these data evidenced direct implications of Gsk-3 for the maintenance of β-cell mass and secretory capacity.
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