| Project/Area Number |
20K09666
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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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| Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
伊東 宏晃 浜松医科大学, 医学部, 教授 (70263085)
内田 季之 浜松医科大学, 医学部附属病院, 准教授 (90570234)
成味 恵 浜松医科大学, 医学部附属病院, 診療助教 (50594321)
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| Project Period (FY) |
2020-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2023: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2022: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2021: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | DOHaD / 慢性炎症 / metaflamation / 胎生期低栄養 / Metaflammation / 胎児期低栄養環境 / 小胞体ストレス / 肝脂肪変性 / エピゲノム |
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| Outline of Research at the Start |
胎生期低栄養マウスモデルにおける、肝細胞内の脂肪滴のサイズが著しく増大し脂肪蓄積の原因としてマイクロアレイの解析よりCell Death-Inducing DNA Fragmentation Factor-Like Effector A (Cidea) およびC (Cidec)が中心的な役割を果たしている可能性に注目し、エピゲノムに着目し解析を行う。
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| Outline of Final Research Achievements |
We focused on endoplasmic reticulum stress as a mechanism involved in the exacerbation of chronic inflammation in tissues due to catch-up growth following prenatal malnutrition, and administered Tauroursodeoxycholic acid (TU), an endoplasmic reticulum stress reliever, in adult animals, and fat weight was significantly reduced. Microarray analysis of adipose tissue identified four Gene Ontologies (GOs) related to inflammation, which were common to both hypofertilization and TU administration. Mφ counts were increased by prenatal malnutrition and decreased by TU administration.
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| Academic Significance and Societal Importance of the Research Achievements |
マウス動物モデルの解析から、胎生期低栄養と出生後のcatch upにより、脂肪組織に炎症に関わる一群の遺伝子発現の変化ならびにマクロファージの集簇が明らかとなった。
二次胆汁酸であるTauroursodeoxycholic acid が、プログラムされたMetaflamtionを改善する可能性が指摘された。Developmental Origins of Metaflamationという新規視点から研究の展開が期待される。
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