| Project/Area Number |
16K11088
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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 |
Obstetrics and gynecology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
平松 祐司 岡山大学, 医歯薬学総合研究科, 特命教授 (80218817)
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| Research Collaborator |
NOBUMOTO Etsuko
MITSUI Takashi
EGUCHI Takeshi
TAMADA Shoko
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | バイオマーカー / 妊娠糖尿病 / 妊娠高血圧症候群 / メタボリック症候群 / プログラミング / 胎生期 / 継代的影響 |
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| Outline of Final Research Achievements |
The links between obesity in parents and their offspring and the role of genes and a shared environment are not completely understood. In this study, we examined whether the offspring from dams exposed to a high fat diet during pregnancy (OH mice) exhibited hypertension, insulin resistance and hyperlipidemia along with epigenetic changes in the expression of adipocytokine genes. Our data demonstrated that the exposure to an HFD in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin and leptin gene expressions.
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| Academic Significance and Societal Importance of the Research Achievements |
母体肥満・耐糖能異常下の子宮内環境による胎児プログラミングの変化がもたらす肥満・耐糖能関連遺伝素因への影響を示す最適なバイオマーカー候補として、アディポサイトカイン遺伝子のエピゲノム変化を同定した。生活習慣病発症を抑制し健やかな次世代育成に繋がる“先制医療”の実用化を目指すためのヒトでの応用を目指す上での端緒となる基盤研究結果と考える。
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