| Project/Area Number |
24658120
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Food science
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| Research Institution | Kyoto Prefectural University |
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Principal Investigator |
KAMEI Yasutomi 京都府立大学, 生命環境科学研究科(系), 教授 (70300829)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | DNAメチル化 / 脂質合成 / 転写調節 / 肝臓 / 授乳期 / エピジェネティクス / メチル化 / インプリント / 肥満 / 脂肪肝 / 遺伝子発現 |
|---|
| Research Abstract |
DNA methylation is a key epigenetic process in the regulation of gene expression in mammals. In this study, we examined the effect of supplementing methionine and specific vitamins (i.e. B12 and folate) to the diet of pregnant/nursing mice on long-term health implications in their offspring. We observed that an early dietary intervention (methyl-supplemented diet) suppressed the increase in body weight and development of a fatty liver induced by a high-fat diet (HFD) in adulthood. We also observed that many genes underwent changes in the DNA methylation levels as a result of the methyl-supplemented diet. C57BL/6J mice are susceptible to HFD-induced obesity. We generated and analyzed reciprocal crosses between 2 mouse strains, namely, F1 progeny with a B6 father and F1 progeny with a PWK father. The former strain was more susceptible to HFD-induced obesity compared with the latter strain; this finding suggested that the susceptibility to HFD-induced obesity was transmitted paternally.
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