| Project/Area Number |
16K15185
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | National Institute for Basic Biology |
|---|
Principal Investigator |
Noda Masaharu 基礎生物学研究所, 統合神経生物学研究部門, 教授 (60172798)
|
|---|
| Research Collaborator |
SHINTANI Takafumi 基礎生物学研究所, 統合神経生物学研究部門, 准教授 (10312208)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
|
|---|
| Keywords | インスリン分泌 / APC2 / 細胞骨格 / 膵β細胞 / 膵島 |
|---|
| Outline of Final Research Achievements |
We found that Apc2-deficeint mice exhibited a higher glucose-induced insulin secretion compared with wild-type mice. Experiments using isolated islets from Apc2-deificient mice and mouse islet cell line MIN6 revealed that APC2 was not implicated in the regulation of insulin secretion at the β-cell level. We found that APC2 was highly expressed in the nerve fibers projecting to pancreatic islets, which suggested that APC2 may play a role in the regulation of insulin secretion through the autonomic nervous system.
|
