| Project/Area Number |
16K09801
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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 |
Endocrinology
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| Research Institution | Osaka University |
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Principal Investigator |
Maeda Norikazu 大阪大学, 医学系研究科, 寄附講座准教授 (30506308)
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| Co-Investigator(Kenkyū-buntansha) |
西澤 均 大阪大学, 医学系研究科, 講師 (20379259)
喜多 俊文 大阪大学, 医学系研究科, 寄附講座講師 (10746572)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アディポネクチン / T－カドヘリン / GPI-PLD / メタボリックシンドローム / 動脈硬化 / 糖尿病 / 肥満 / T-カドヘリン / 内分泌学 |
|---|
| Outline of Final Research Achievements |
A series of our studies find out the following novel mechanism. Adiponectin, an adipocyte-specific secretory circulating protein, suppresses the development of atherosclerosis through T-cadherin, a GPI-anchored cell surface protein. Adiponectin binds to specific domain of T-cadherin with high affinity.
We also discover the novel mechanism explaining the variety of organ protective role of adiponectin. Adiponectin significantly enhances the exosome production via T-cadherin.
We furthermore demonstrate that GPI-PLD, a GPI-anchor cleavage enzyme, is significantly increased especially in liver, and GPI-PLD knockout mice escape from diet-induced diabetes, suggesting that GPI-PLD inhibitors will be useful for novel therapeutic tools against diabetes.
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| Academic Significance and Societal Importance of the Research Achievements |
アディポネクチンがT-カドヘリンを介して動脈硬化はじめ様々な臓器に対して保護作用を発揮する機序を本研究により明らかに出来たことで、新たな治療薬の開発に繋がる可能性が導かれた。
GPI-PLDは酵素であるため、その阻害薬の開発は比較的容易であり、本研究により新たな糖尿病治療展開が期待される。
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