Investigation of roles of GSK-3β in the regulation of pancreatic β cell mass for the application to the treatment of type 2 diabetes mellitus.
| Project/Area Number |
22590984
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Yamaguchi University |
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Principal Investigator |
TANABE Katsuya 山口大学, 医学部附属病院, 助教 (00397994)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| 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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| Keywords | エネルギー / 糖質代謝異常 / 糖尿病 / 膵β細胞 / GSK-3 / 小胞体ストレス / 2型糖尿病 / Gsk-3β / インスリンシグナル |
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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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Report
(4 results)
Research Products
(26 results)
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[Journal Article] Glucose and fatty acids synergize to promote B-cell apoptosis through activation of glycogen synthase kinase 3β independent of JNK activation2011
Author(s)
Tanabe K, Liu Y, Hasan SD, Martinez SC, Cras-Meneur C, Welling CM, Bernal-Mizrachi E, Tanizawa Y, Rhodes CJ, Zmuda E, Hai T, Abumrad NA, Permutt MA
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Journal Title
PLoS One
Volume: 26
Issue: 4
Pages: e18146-e18146
DOI
Related Report
Peer Reviewed
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