| Project/Area Number |
21390451
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Mie University |
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Principal Investigator |
SAGAWA Norimasa 三重大学, 大学院・医学系研究科, リサーチアソシエイト (00162321)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Takashi 三重大学, 医学部附属病院, 准教授 (10263005)
UMEKAWA Takashi 三重大学, 医学部附属病院, 助教 (80422864)
KAMIMOTO Yuki 三重大学, 医学部附属病院, 助教 (90422865)
MURABAYASHI Nao 三重大学, 医学部附属病院, 助教 (10378416)
MIZOGUCHI Akira 三重大学, 大学院・医学系研究科, 教授 (90181916)
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| Co-Investigator(Renkei-kenkyūsha) |
YURA Shigeo 京都大学, 大学院・医学研究科, 講師 (60335289)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2011: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2010: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2009: ¥10,400,000 (Direct Cost: ¥8,000,000、Indirect Cost: ¥2,400,000)
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| Keywords | 妊娠 / 子宮内環境 / 胎児プログラミング / 成人病 / 糖脂質代謝 / インスリン抵抗性 / 高血圧 / 脂肪組織の慢性炎症 / 高脂肪食 / 肥満 / 生活習慣病 / アディポカイン / 耐糖能異常 / 胎生期低栄養 / 糖代謝異常 / マクロファージ |
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| Research Abstract |
The aim of this study was to confirm the fetal origins of adult disease hypothesis and to explore a tool to prevent adult diseases of fetal origins. We found that hypertension in the offspring exposed to under nutrition in utero was closely related to activation of cardiac angiotensin system and that development of hypertension in these offspring was blocked by feeding high protein diet or branched chain amino acid to the pregnant mother. Maternal obesity is another cause of perinatal morbidity such as gestational diabetes and pregnancy-induced hypertension. Therefore, we also examined the effect of maternal high-fat diet on both mother and fetus. We found that high fat diet caused not only maternal obesity and impaired glucose tolerance but also hypertension and impaired glucose tolerance in the next generation through chronic inflammation of fat tissue of the fetus.
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