| Project/Area Number |
17591137
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
NAGAYA Ken (2006-2007) Asahikawa Medical College, Department of Pediatrics, assistant professor (80396382)
竹田津 原野 (2005) 旭川医科大学, 医学部, 助手 (10360992)
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| Co-Investigator(Kenkyū-buntansha) |
MAKITA Yoshio Asahikawa Medical Collage, Education center, professor (20271778)
HAYASHI Tokitsugu Asahikawa Medical Collage, Department of Pediatrics, lecturer (40322911)
FUJIEDA Kenji Asahikawa Medical Collage, Department of Pediatrics, professor (60173407)
長屋 建 旭川医科大学, 大学病院, 医員 (80396382)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | gene / medical / genome / intrauterine growth retardation / growth fator / 胎児発育 / insulin-like gorwth factor I / insulin-like growth factor II / type 1 insulin-like growth factor receptor / 遺伝的多い型 / SNP / 子宮内胎児発育遅延 / ハプロタイプ |
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| Research Abstract |
Objective Insulin like growth factors (IGF1 and IGF2) and their receptors (IGF1R and IGF2R) associate with feto-placental growth. We hypothesized that polymorphism of IGFs gene could alter birth weight and placental weight inhuman.
Subject and methods: The healthy 287 infants without congenital anomaly, who were born at〓35 weeks of gestational agebetween October 2004 and September 2007 in our hospital and Mori obstetrics gynecology hospital and their mothers were examined about IGFs and their receptors genes. We carried out haplotype analysis between feto-placental growth and IGF1, IGF2, IGF1R and IGF2R. Moreover, we analyzed methylation status of infants IGF2 gene using Mass ARRAY. Moreover, we compared their anthropometric status at 18 month of age according to haplotypes of IGF2.
Result: Frequency of IGF1 haplotype TGG in heavy for date (HFD) infants was significantly higher than in appropriate for date (AFD) or small for date (SFD) infants. Infants with IGF1 haplotype TGG were significantly heavier birth weight compared with that of non-TGG infants. Hence, frequency of haplotype CTG of paternal IGF2 allele in SFD infants was significantly higher than in AFD or HFD infants. Infants with IGF2 haplotype CTG were significantly shorter birth length, lighter birth weight and placental weight compared with those of non-CTG infants. There was no significant difference in cord serum IGF-2 level regardless of haplotypes. Moreover, haplotype CTG on IGF2 gene did not associate with its methylation status. The infants with IGF2 haplotype CTG caught up their anthropometric status as much as that of non-CTG infants.
Conclusion: IGF1 haplotype TGG may associate with increase of fetal growth. Haplotype CTG of paternal allele on IGF2 gene may reduce feto-placental growth regardless of its mathylation status, but not associate postnatal growth.
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