2011 Fiscal Year Final Research Report
Molecular mechanism of ER stress response by alcohol abuse.
| Project/Area Number |
22790597
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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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) |
2010 – 2011
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| Keywords | アルコール / 小胞体ストレス / 臓器障害 |
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| Research Abstract |
To clarify the molecular mechanism of endoplasmic reticulum(ER) stress response by alcohol abuse, I focused on the lipid accumulation and lipid metabolism, both observed nearby ER. Creatine is one of factors concerning lipid metabolism. I had to establish new lab system for primary rat hepatocyte culture, because of moving on new institutes. I checked the condition of culture in the new system. I performed primary rat hepatocyte culture and loaded 0-100 mM ethanol in the culture medium with 0-10% serum for 24 hours. I found that ethanol suppressed serum concentration of creatinine, which converted from creatine and increased depending on the concentration of serum in the culture medium. Creatine is synthesized in the liver and creatine plays important role in lipid metabolism. Alcohol may suppress creatine synthesis in the liver leading disturbance of ER stress response and alcoholic liver disease.
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