| Project/Area Number |
25460879
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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 |
Legal medicine
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AKIMOTO Toshio 日本医科大学, 医学部, 准教授 (30184112)
MARUYAMA Motoyo 日本医科大学, 医学部, 助教 (60709757)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | アルコール代謝 / ADH1 / ADH3 / アルコール嗜好性 / アルコール肝障害 / アルコール依存 / ノックアウトマウス / 慢性アルコール摂取 / アルコール性肝障害 / アルコール依存症 / ピラゾール感受性 / 社会医学 / アルコール医学 / アルコール脱水素酵素 / アルコール代謝亢進 / アルコール性脂肪肝 / 急性アルコール投与 |
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| Outline of Final Research Achievements |
Three kinds of mice with different ADH genotypes(Wild, Adh1-/-, Adh3-/-) were subjected under chronic alcohol consumption（CAC) with 10% ethanol. ADH1 was found to be indispensable to continue CAC, and to have protective roles in alcoholic liver disease and dependence. On the other hand, ADH3 was demonstrated to accelerate alcoholic liver disease and alcoholism, although it represses daily alcohol intake under CAC. It is also suggested that both ADHs contribute to an increase in alcohol metabolism by CAC, especially in the absence of the other one, however, the contribution of ADH1 decrease in the prolonged CAC, differing from that of ADH3.
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