| 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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| 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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