Analysis of epigenomic modification of fetal liver caused by maternal nutrition via endoplasmic reticulum signal
| Project/Area Number |
15K19023
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ZHANG Jun 徳島大学, 先端酵素学研究所(プロテオ), 特任研究員 (70629790)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 分子病態栄養学 / 小胞体ストレス / PERK |
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| Outline of Final Research Achievements |
Epidemiological studies have revealed that the nutritional status of pregnant mothers is related to an increase the risk for adverse outcomes both in maternal and offspring health, but a detailed molecular mechanism is still unknown. Previously, we have found that PERK, which regulates endoplasmic reticulum stress response, is activated by changes in nutritional conditions such as starvation and satiation, and that activation of PERK affects glucose metabolism and lipid metabolism in the liver. In this study, epigenomic changes in fetal liver via PERK were analyzed using genetically modified mice which can arbitrarily activate only PERK in the liver. We found that the proportion of DNA methylation was increased in the liver after birth when PERK was activated in the liver at a time of embryonic stage.
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Report
(3 results)
Research Products
(8 results)
