| Project/Area Number |
18380083
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Kyushu University |
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Principal Investigator |
IMAIZUMI Katsumi Kyushu University, Fac. of Agriculture, Professor (90037466)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Masao Kyushu University, Fac. of Agriculture, Associate Professor (90294909)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,380,000 (Direct Cost: ¥15,300,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2007: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2006: ¥11,700,000 (Direct Cost: ¥11,700,000)
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| Keywords | mevalonic acid / fatty acid synthetase / metabolic imprinting / DNA methylation / 脂肪酸合成酵素 / プロモーター領域 / DNAのメチル化 |
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| Research Abstract |
It was reported that nutritional environments in an early stage of life affects on metabolism 'in the latter life. This phenomenon is called as "Metabolic imprinting".
In our previous study, rat pups fed a diet rich in mevalonic acid (MA) for 3weeks, after growing, had such characters as low hepatic triacylglycerol (TG) and fatty acid synthetase (FAS) mRNA levels compared to a control diet without MA.
These results suggest that dietary MA has an effect of a metabolic imprinting as reducing hepatic TG and FAS mRNA levels. This research's aim was to revail mechanism(s) for the metabolic imprinting by dietary MA.
We tried to use HepG2 cells of hepatic carcinoma cells to ensure the in vivo result. HepG2 cells under 80% confluent condition were exposed to medium containing MA for 36 hours, and then were cultured by medium without MA for 36 hours. Control cells were cultured for 72 hours. Comparing to the control cells, in the test cells, the FAS mRNA levels was lower this result consistent with the in vivo result.
Next, we investigated a mechanism of an expression of this phenomenon, in which focusing on DNA methylation occurs in CpG islands in promoter of genes. In the same condition of the cultivated cells as described before, we measured ratios of CpG methylation in FAS promoter region.
As the results, MA promotes the methylation of CpG around sterol .regulatory element. These results suggest that MA temporary exposure to HepG2 cells promotes methylation in its promoter region of FAS to suppress expression of FAS mRNA.
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