2018 Fiscal Year Final Research Report
The role of Epac2A/Rap1 signaling in the protection of pancreatic beta-cell
| Project/Area Number |
16K09749
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Kobe University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 膵β細胞 / 糖尿病 / インクレチン / cAMP / Epac2 |
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| Outline of Final Research Achievements |
The roles of incretin/cAMP signaling and Epac2/Rap1 signaling in the protection of pancreatic β-cells were investigated. In a β-cell line, the activation of cAMP and Epac2 signaling suppressed production of reactive oxygen species (ROS) induced by alloxan and palmitate stimulations, suggesting that the role of cAMP and Epac2 signaling in the reduction of oxidative stress in pancreatic β-cells. From the generation and analyses of Epac2 deficient cell lines, we found a new isoform of Epac2 expressed in pancreatic β-cells, which may be involved in cellular functions other than insulin secretion such as the protection of β-cell against cellular stresses including oxidative stress.
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| Free Research Field |
代謝学
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| Academic Significance and Societal Importance of the Research Achievements |
インクレチンは食餌の摂取によって腸管から分泌され、膵β細胞からのインスリン分泌を促進するなど、糖代謝改善作用を有する。この作用を利用したインクレチン関連薬は現在２型糖尿病治療に広く用いられており、その作用機序や未知の効果を明らかにすることは臨床上の意義が大きい。また、糖尿病の病態には各種細胞ストレスなどによる膵β細胞機能の障害が深く関与しており、このような病態の解明により新規糖尿病治療法の開発にも繋がる可能性があることから本研究の意義は大きい。
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