| Project/Area Number |
22790842
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | Nihon University (2011)
Tohoku University (2010) |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 膵β細胞 / 小胞体ストレス / 4E-BP1 / ATF6α / DPP-4阻害薬 / 糖尿病 |
|---|
| Research Abstract |
In the current study, we investigated 4E-BP1 expression, which is important for beta-cell survival, in MIN6 cells under ER stress and oxidative stress. We found that JNK activated by oxidative stress is involved in the modulation of 4E-BP1 expression and phosphorylation in MIN6 cells.
In this study, we analyzed Atf6α-null mice. ATF6α protects β-cells from ER stress and suppresses hepatosteatosis, but plays a role in the development of hyperlipidemia and insulin resistance.
The study is designed to investigate whether the activation of the incretin system by DPP-4 inhibition ameliorates β-cell failure in WFS1-deficient mice, a genetically defined model of human diabetes caused by ER stress in β-cells. These findings provide evidence that activation of the incretin system by vildagliptin plays a protective role against β-cells with WFS1-deficiency.
|
