Epigenetic control of gene expression associated with adult diseases due to fetal nutritional factors
Project/Area Number |
21591409
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
|
Research Institution | Tohoku University |
Principal Investigator |
MUROTSUKI Jun 東北大学, 大学院・医学系研究科, 非常勤講師 (50239555)
|
Co-Investigator(Kenkyū-buntansha) |
SATO Kazuyo 東北大学, 大学院・医学系研究科, 非常勤講師 (70375020)
ARAKI Yoshihiko 順天堂大学, 環境医学研究所, 准教授 (70250933)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | DOHaD仮説 / 低タンパク食 / メチル化 / エピジェネティクス / 妊娠マウス / DOHaD / 2013/10/04 / SPHK-1 / epigenetics / metabolic disease / 胎児発育遅延 / 成人病 / 子宮内環境 / マウス |
Research Abstract |
One likely mechanism of the developmental origins hypothesis is via early nutritional influences on epigenetic gene modification consisting of the presence of a methyl group on the carbon 5 of a cytosine residue. We have tested the hypothesis that maternal low-protein diet altered epigenetic regulation of specific gene of the offspring. Hepatic Oct-4 or Sphk-1 methylation pattern of the genomic DNA is specific in low-protein diet group. Aberrant Oct-4 and Sphk-1 gene expression may cause perturbations in cell differentiation. We suggest that the epigenetic mechanism consisting of DNA methylation underlies the fetal programming theory.
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Report
(4 results)
Research Products
(13 results)