| Project/Area Number |
18K19726
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
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| Research Institution | Kyoto University (2019)
Gunma University (2018) |
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Principal Investigator |
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2018: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 飲酒 / FGF21 / オキシトシン / 嗜好性 / SIRT1 / 飲酒欲求 / 希少糖 / アルコール |
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| Outline of Final Research Achievements |
Alcohol dependence is a major health burden, but the treatment options are limited. Therefore, we aimed to elucidate the molecular and neural basis that regulates alcohol preference, focusing on FGF21, oxytocin, and SIRT1.
We found that overexpression of SIRT1 specifically in the nervous system or in the oxytocin neurons significantly suppressed alcohol preference in mice. However, deleting SIRT1 specifically in the nervous system or in the oxytocin neurons did not affect alcohol preference in mice.
Feeding mice a SIRT1 activator resveratrol for 2 weeks significantly suppressed alcohol preference in the wild-type mice. However, supplementing a precursor of NAD+, a co-factor for SIRT1 activity, nicotinamide mononucleotide (NMN) for 2 weeks did not affect alcohol preference in the wild-type mice.
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| Academic Significance and Societal Importance of the Research Achievements |
アルコール嗜好性を制御する新たな分子・神経基盤を解明し、特許出願を行った。SIRT1の活性化剤の長期投与により、アルコール嗜好性を抑制できる可能性は示すことが出来たが、同様の作用機序が推察される前駆体補充療法では有意な効果が得られなかったため、SIRT1を分子標的にしてアルコール嗜好性を抑制することは、現実的には難しいのではないかとの結論に至った。
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