| Project/Area Number |
15K18394
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Research Collaborator |
TANAKA Hiroki
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 鉄過剰 / エピジェネティクス / DNAメチル化 / 糖代謝 |
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| Outline of Final Research Achievements |
In the study, we found that the enzymes associated with glucose metabolism were increased in the iron overloaded mice that received short-term iron overload. Furthermore, 2-hydroxyglutarate (2-HG), which was aberrant metabolites in the TCA cycle, was increased in the iron overloaded mice. Furthermore, the 2-HG production resulted in upregulation of DNA methylation in the iron overloaded mice. From these results, we considered that DNA methylation were increased by iron overload through enhancement of the abnormal glucose metabolism.
On the other hands, when we performed similar analysis using long-term iron overload model mice, DNA methylation were rather decreased in the iron overloaded mice. To know the detailed mechanism during iron overload, we need further analysis by focusing the period of iron overload.
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