| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Low-birth weight resulted from intrauterine growth retardation is thought to be a risk factor of adult diseases such as diabetes, obesity and cardiovascular disfunction according to the Fetal Origin of Adult Diseases Theory. However, how the intrauterine growth retardation leads the infant susceptible to adulthood disease is not well understood. We have shown that when C.elegans, a widely used experimental model of multi-cellular organism, was deprived of food, their progeny accumulated more fat than their counterpart, indicating C.elegans can be a good model for analyzing Fetal Origin of Adult Diseases Theory.
We have shown that genes involved in methylation of certain lysine residues in H3 histone are differentially expressed in worms derived from starvation-experienced worms compared to those of worms derived from fed-worms. Our result indicates that epigenetic modification in histone may be responsible for Fetal Origin of Adult Diseases Theory.
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