| Project/Area Number |
24591610
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Keio University |
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Principal Investigator |
HIDA MARIKO 慶應義塾大学, 医学部, 共同研究員 (20276306)
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| Co-Investigator(Kenkyū-buntansha) |
AWAZU Midori 慶應義塾大学, 医学部, 講師 (20129315)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 胎児プログラミング / 子宮内胎児発育遅滞 / oligomeganephronia / 生活習慣病 / 慢性腎疾患 / 子宮内胎児プログラミング / 尿細管分岐 / 胎内プログラミング / 腎機能障害 / 尿細管障害 |
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| Outline of Final Research Achievements |
The number of low birth weight babies, products of intra uterine growth retardation (IUGR), is increasing in Japan. Those IUGR survivors are known to develop metabolic syndrome in adult life due to probable reduced kidney function. We studied glomerular and tubular function of 53 extremely low birth weight subjects (ELBW). Twenty five percent of subjects had glomerular dysfunction and eighty three percent of them had tubular dysfunction. We showed that maternal nutritional restriction, NR, leads to reduced ureteric branching resulted in low nephron number of rat embryos. In those embryos, DNA methylation of genes involved in ureteric branching has been changed, which may contribute to reduced nephron number and transgenerational transmission. Further, we found the kidney of offsprings from NR rats were more susceptible to ischemia and fibrosis secondary to unilateral ureteral obstruction.The results have pointed out necessity of careful follow-up of kidney function for those premies.
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