| Project/Area Number |
24590860
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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 | Kumamoto University |
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Principal Investigator |
NISHITANI Yoko 熊本大学, 大学院生命科学研究部, 教授 (30359997)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 法医学 / アルコール医学 / 肝臓 / エタノール / 小胞体ストレス / アルコール / 肝細胞 / クレアチン / クレアチン産生 |
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| Outline of Final Research Achievements |
To clarify the mechanism of alcohol induced organ injury, we focused on the creatine production in hepatocytes. Creatine is produced in hepatocytes and related with energy metabolism. Ethanol reduced the creatinine, which is created from creatine, in the medium of primary rat hepatocyte culture, and 4-MP, an alcohol dehydrogenase inhibitor, recover the reduction. Ethanol also reduced acetone, one of the ketone body produced during the fatty acid oxidation. SIRT1 is related to NAD dependent deacetylation of the protein that related creatine production. Howerver, there was no effect of SIRT1 activator on the ethanol metabolism or acetone concentration. Ethanol and its metabolism may affect the lipid oxidation and creatine production, even though it is necessary to study more details.
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