2017 Fiscal Year Final Research Report
The role of maternal insulin resistance and lipase activity on fetal growth
Project/Area Number |
26461644
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
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Research Institution | Juntendo University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
横山 和仁 順天堂大学, 医学部, 教授 (00158370)
竹田 省 順天堂大学, 医学部, 特任教授 (20143456)
北村 文彦 順天堂大学, 医学部, 准教授 (20301145)
松川 岳久 順天堂大学, 医学部, 助教 (60453586)
西岡 笑子 順天堂大学, 医学部, 非常勤講師 (70550797)
牧野 真太郎 順天堂大学, 医学部, 准教授 (70570894)
三井田 孝 順天堂大学, 医学(系)研究科(研究院), 教授 (80260545)
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Research Collaborator |
UENO Tsuyoshi 順天堂大学, 医学部, 協力研究員
KON Mika 順天堂大学, 医学部, 大学院生
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Project Period (FY) |
2014-04-01 – 2018-03-31
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Keywords | リポ蛋白リパーゼ / インスリン抵抗性 / 妊娠 / 臍帯血 / 胎児発育 / 脂質異常症 |
Outline of Final Research Achievements |
Triglyceride-rich lipoprotein (TGRL) is catabolized to glycerol and free fatty acid (FFA) by the action of lipoprotein lipase (LPL). During pregnancy, FFA passes through the placenta and is used for fetal growth and development. Because insulin resistance inhibits maternal LPL activity, catabolism of TGRL is suppressed. Therefore, it is uncertain whether fetus can efficiently obtain FFA from maternal TGRL in gestational period. This study indicates that 1) insulin resistance affects glucose and lipid metabolism during pregnancy, 2) maternal LPL concentration decreases by about 28~35% because of insufficient insulin action, 3) mean LPL concentration in cord blood is about two holds higher than that in maternal blood during the second trimester and positively correlated with birthweight. These results suggest that LPL from placenta may compensate decrease of maternal LPL action, and promote fetus growth during pregnancy.
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Free Research Field |
医歯薬学
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