Elucidation of the pathogenic mechanism of testicular dysfunction due to malnutrition during the embryonic period
Project/Area Number |
17K10074
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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 |
Pediatrics
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Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
Fujisawa Yasuko 浜松医科大学, 医学部附属病院, 講師 (40402284)
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Project Period (FY) |
2017-04-01 – 2021-03-31
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Project Status |
Completed (Fiscal Year 2020)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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)
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Keywords | 胎生期低栄養環境 / 精巣機能低下 / 低アンドロゲン / DoHAD / 胎生期低栄養 / DOHaD / 精巣異形成症候群 / エピゲノム / ライディッヒ細胞 / 母体低栄養 / 子宮内発育遅延 / 精巣機能不全 / 胎生期プログラミング / 精巣 / 性分化 |
Outline of Final Research Achievements |
We conducted a study to examine the mechanism of "undernutrition environment during the embryonic period causes postnatal testicular dysfunction and reproductive dysfunction". As a result of examining pregnant mice by dividing them into two groups, a free feeding group (C group) and a nutritionally restricted group (R group), a decrease in testosterone in the fetal testis, and sperm count at 6 weeks of age in R mothers. A decrease in numbers was revealed. From the above results, a new disease-onset theory of post-growth sperm count decrease due to low androgen state induced in the embryonic malnutrition environment was clarified. Furthermore, we are proceeding with whole-genome methylome of isolated Leydig cells.
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Academic Significance and Societal Importance of the Research Achievements |
近年、男性生殖器疾患の発症頻度は増加しています。その理由は様々ですが、なんらかの胎児期の環境因子の影響が考えられています。私たちは、母体の低栄養環境が生後の男性精巣機能の障害に関与する可能性を考え、マウスを使った実験にて検証を行いました。その結果、1母マウスの低栄養状態が胎児(胎仔)マウス精巣における男性ホルモン(テストステロン)の濃度を低下させる こと 2低栄養母マウスから出生した雄マウスでは、生後6週の時点で精子数が減少すること、が明らかになりました。以上から、私たちは胎生期低栄養環境に惹起された低男性ホルモン状態に起因する男性生殖器障害という新しい疾病発症セオリーを提唱します。
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Report
(5 results)
Research Products
(9 results)
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[Journal Article] Paradoxical gain-of-function mutant of the G-protein-coupled receptor PROKR2 promotes early puberty.2017
Author(s)
Fukami M, Suzuki E, Izumi Y, Torii T, Narumi S, Igarashi M, Miyado M, Katsumi M, Fujisawa Y, Nakabayashi K, Hata K, Umezawa A, Matsubara Y, Yamauchi J, Ogata T.
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Journal Title
Journal of Cellular and Molecular Medicine
Volume: -
Issue: 10
Pages: 2623-2626
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] FGFR1 Analyses in Four Patients with Hypogonadotropic Hypogonadism with Split-Hand/Foot Malformation: Implications for the Promoter Region.2017
Author(s)
Ohtaka K, Fujisawa Y, Takada F, Hasegawa Y, Miyoshi T, Hasegawa T, Miyoshi H, Kameda H, Kurokawa-Seo M, Fukami M, Ogata T.
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Journal Title
Hum Mutat.
Volume: 38
Issue: 5
Pages: 503-506
DOI
Related Report
Peer Reviewed
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