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Analysis of the paternal transmission of obesity.

Research Project

Project/Area Number 16K07194
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Genome biology
Research InstitutionGunma University

Principal Investigator

Morita Sumiyo  群馬大学, 生体調節研究所, 助教 (40589264)

Co-Investigator(Kenkyū-buntansha) 畑田 出穂  群馬大学, 生体調節研究所, 教授 (50212147)
Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Keywords肥満 / 父性遺伝 / インプリンティング / ゲノムインプリンティング / エピジェネティクス / エピゲノム
Outline of Final Research Achievements

We found that B6 mice are more prone to develop obesity than PWK mice, and we analyzed reciprocal crosses between these mice and found that (PWK × B6) F1 mice, which have B6 fathers, are more likely to develop dietary obesity than (B6 × PWK) F1 mice, which have B6 mothers. In addition, we performed transcriptome analysis of adipose tissues of these mice using next-generation sequencing. We found that paternal transmission of diet-induced obesity was correlated with genes involved in adipose tissue inflammation, metal ion transport, and cilia.
Furthermore,we found that expression of paternally expressed imprinted genes (PEGs) was down-regulated in the obesity-prone B6 mice by a high-fat diet,suggesting that abnormally low expression of PEGs contributes to high-fat diet-induced obesity in B6 mice.

Academic Significance and Societal Importance of the Research Achievements

C57BL/6 (B6)マウスは高脂肪食を食べさせることにより肥満になりやすいが、その遺伝的背景についてはわかっていない。今回の研究では食事誘導性肥満になりやすいB6と食事誘導導性の肥満になりにくいPWKを交互に交配して2種類のF1をつくり肥満とインプリンティングの関係について調べた。B6が父親のとき、すなわち(PWK×B6) F1は食事誘導性肥満になりやすく耐糖能異常を示すが、PWKが父親のときは、すなわち(B6×PWK) F1では肥満にもなりにくく耐糖能異常も示さなかった。つまり食事誘導性肥満、耐糖能異常は父性遺伝することがわかった

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (5 results)

All 2018 2016 2015

All Journal Article (3 results) (of which Peer Reviewed: 2 results,  Open Access: 2 results) Presentation (2 results)

  • [Journal Article] Editing of DNA Methylation Using dCas9-Peptide Repeat and scFv-TET1 Catalytic Domain Fusions2018

    • Author(s)
      Morita Sumiyo、Horii Takuro、Hatada Izuho
    • Journal Title

      Methods Mol Biol.

      Volume: 1767 Pages: 419-428

    • DOI

      10.1007/978-1-4939-7774-1_23

    • ISBN
      9781493977734, 9781493977741
    • Related Report
      2018 Annual Research Report 2017 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] 肥満のエピジェネティクスとその世代間継承2016

    • Author(s)
      畑田出穂、森田純代
    • Journal Title

      実験医学増刊, エピゲノム研究 修飾の全体像の理解から先制・個別化医療へ, 羊土社

      Volume: 34 Pages: 1617-1621

    • Related Report
      2016 Research-status Report
  • [Journal Article] Gene expression profiling of white adipose tissue reveals paternal transmission of proneness to obesity.2015

    • Author(s)
      Morita S, Nakabayashi K, Kawai T, Hayashi K, Horii T, Kimura M, Kamei Y, Ogawa Y, Hata K, Hatada I
    • Journal Title

      Sci. Rep.

      Volume: 6 Issue: 1 Pages: 21693-21693

    • DOI

      10.1038/srep21693

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] エピゲノム編集:特定のDNAメチル化領域を効率よく操作する方法の開発2018

    • Author(s)
      森田純代、堀居拓郎、木村美香、畑田出穂
    • Organizer
      日本分子生物学会
    • Related Report
      2018 Annual Research Report
  • [Presentation] 父性遺伝する食事誘導性肥満におけるインプリント遺伝子の解析と新規インプリント遺伝子の探索について2016

    • Author(s)
      森田純代、中林一彦、河合智子、林恵子、堀居拓郎、木村美香、、亀井康富、小川佳宏、秦健一郎、畑田出穂
    • Organizer
      日本エピジェネティックス研究会第10回年会
    • Place of Presentation
      千里ライフサイエンスセンター
    • Year and Date
      2016-05-19
    • Related Report
      2016 Research-status Report

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Published: 2016-04-21   Modified: 2020-03-30  

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