Fatty acid dynamics as insulin secretion capacity regulating factor: analysis in new model mice
Project/Area Number |
17K08780
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Tohoku University |
Principal Investigator |
Asai Akira 東北大学, 農学研究科, 特任准教授 (30500011)
|
Co-Investigator(Kenkyū-buntansha) |
杉原 仁 日本医科大学, 大学院医学研究科, 大学院教授 (60183414)
都築 毅 東北大学, 農学研究科, 准教授 (00404848)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | インスリン分泌 / 膵島 / β細胞 / 脂肪酸 / CD36 / 糖尿病 / モデルマウス / 2型糖尿病 |
Outline of Final Research Achievements |
Pancreatic islets were isolated from diabetes-prone (Prone) and diabetes-resistant (Resistant) mice, and used for each analysis. There are heritable differences in insulin secretion capacity between the two lines of mice. Many differences were observed in gene expression of molecules involved in metabolism and transport of fatty acids and lipids. We found that different expression levels of CD36, known as a fatty acid transporter on plasma membrane, in pancreatic beta cells may determine the heritable differences in insulin secretion capacity.
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Academic Significance and Societal Importance of the Research Achievements |
Prone系とResistant系の両系統マウスは、多遺伝子性の遺伝的要因と環境的要因との相互作用というヒトにおける2型糖尿病発症基盤を正しく反映して作出されたモデル動物である。両系統間での遺伝的なインスリン分泌能の差異について、その出現機序の解明を目的とした本研究の成果は、ヒトにおける2型糖尿病の発症基盤や発症における個人差の成因解明、さらには、それらに基づいた糖尿病予防・治療法開発に繋がる基礎的知見となるものと考えられる。
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Report
(4 results)
Research Products
(14 results)