| Project/Area Number |
17K00880
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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 |
Eating habits
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| Research Institution | Josai University (2020-2022)
Juntendo University (2017-2019) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
長岡 功 順天堂大学, 大学院医学研究科, 教授 (60164399)
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| Project Period (FY) |
2017-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | グルコサミン / 散骨細胞 / オートファジー / 軟骨細胞 / 変形性関節症 / サーチュイン / 機能性食品 |
|---|
| Outline of Final Research Achievements |
Glucosamine (GlcN), a naturally occurring amino monosaccharide, has been widely used to treat osteoarthritis (OA) in humans. However, the effects of GlcN on autophagy in chondrocyte are still unknown. In this study, to elucidate the chondroprotective action of GlcN via autophagy, we evaluated the effect of GlcN on the expression of autophagy-related molecules (LC3-II, Beclin-1, ATG5 and ATG7) using a human chondrocyte. GlcN significantly increased protein level of LC3-II and mRNA expression of Beclin-1, ATG5 and ATG7. Moreover, GlcN significantly increased the protein level of SIRT1. Importantly, the GlcN-induced increase of LC3-II protein was inhibited by EX527 (a SIRT1 inhibitor). Moreover, GlcN did not effect the S6K phosphorylation, as a target of mammalian target of rapamycin (mTOR). Together these observations suggest that GlcN increases the expression of SIRT1 and possibly induces autophagy in chondrocytes independent of mTOR, thereby exhibiting the chondroprotective action.
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| Academic Significance and Societal Importance of the Research Achievements |
軟骨細胞において、グルコサミンがオートファジーを誘導するという新規機能を解明した。さらに、その誘導経路がmTOR非依存的な経路であることも示した。このことは、グルコサミンの新規機能を明らかにしただけでなく、軟骨を標的とした今後の新薬の発見にもつながることが期待される。
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