The role of nuclear DGKdelta on lipid signaling in pancreatic beta-cells and its involvement in the pathogenesis of type 2 diabetes mellitus.
| Project/Area Number |
26750336
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied health science
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| Research Institution | University of Shizuoka |
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Principal Investigator |
Kaneko Yukiko 静岡県立大学, 薬学部, 講師 (00381038)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 糖尿病 / 膵β細胞 / ジアシルグリセロール / ジアシルグリセロールキナーゼ / 細胞増殖 / インスリン分泌 / 脂質シグナリング |
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| Outline of Final Research Achievements |
In the present study, we investigated the role of diacylglycerol kinase δ (DGKδ) on the function of pancreatic β-cells. The expression of DGKδ was detected in the nucleus of β-cells. To explore the function of DGKδ in pancreatic β-cells, we used a Cre/loxP system to create mice with β-cell specific disruption of DGKδ (βDGKδKO). βDGKδ KO showed lower blood glucose and higher plasma insulin levels compared with the control mice and improvement of glucose tolerance. βDGKδ KO also showed an increase in the number of small islets. Moreover, the deficiency of DGKδ in β-cells led to a significant decrease in the progression of streptozotocin-induced hyperglycemia and β-cell loss. Based on the present results, we propose that the inhibition of DGKδ, which acts as a suppressor of β-cell proliferation, could be a novel therapeutic target for diabetic mellitus.
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Report
(4 results)
Research Products
(43 results)
