| Project/Area Number |
17591730
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kyoto University |
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Principal Investigator |
YURA Shigeo Kyoto University, Graduate School of Medicine, assistant professor, ・医学研究科, 助手 (60335289)
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| Co-Investigator(Kenkyū-buntansha) |
SAGAWA Norimasa Mie University, Graduate School of Medicine, professor, 医学系研究科, 教授 (00162321)
ITOH Hiroaki Kyoto University, Graduate School of Medicine, lecturer, ・医学研究科, 講師 (70263085)
MASUZAKI Hiroaki Kyoto University, Graduate School of Medicine, assistant professor, ・医学研究科, 助手 (00291899)
YORIFUJI Toru Kyoto University, Graduate School of Medicine, lecturer, ・医学研究科, 講師 (60220779)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | IUGR / neonatal leptin surge / glucocorticoid / maternal food restriction / intrauterine undernutrition / IUGR / 摂餌制限 / 脂質代謝障害 / 栄養 |
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| Research Abstract |
Intrauterine fetal growth restriction (IUGR) is one of major pathologies during pregnancy, which is often associated with fetal or neonatal mortality and morbidity. Recent epidemiological study revealed that IUGR is also associated with adulthood metabolic disorders after neonatal catch up growth. In the present study, we used mice model of intrauterine undernutrition to evaluate energy metabolism in IUGR fetus. In IUGR offspring by maternal food restriction during pregnancy, impaired glucose tolerance and accelerated weight gain on a high fat diet was observed in adulthood. It was revealed that premature neonatal leptin surge in these offspring may play a role in the development of such adulthood metabolic disorders. In IUGR offspring, fatty liver and abnormal gene expression in the adipose tissue were also demonstrated in adulthood. These findings may help us to understand mechanisms of development of metabolic disorders in IUGR fetus. On the other hand, glucocorticoid has various effect on fetal metabolism and growth. In order to elucidate effects of increased glucocorticoid concentrations on fetal growth in pregnant mice with food restriction, we examined maternal food intake and fetal growth after glucocorticoid administration to pregnant mice. Glucocorticoid administration increased maternal food intake but suppressed fetal growth. Placental and fetal hepatic IGF-I expression were increased by glucocorticoid administration, thus suggesting that fetal growth suppression is mediated through other mechanisms than increment of IGF-I signal.
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