Analysis of the paternal transmission of obesity.
| Project/Area Number |
16K07194
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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 |
Genome biology
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| Research Institution | Gunma University |
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Principal Investigator |
Morita Sumiyo 群馬大学, 生体調節研究所, 助教 (40589264)
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| Co-Investigator(Kenkyū-buntansha) |
畑田 出穂 群馬大学, 生体調節研究所, 教授 (50212147)
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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 |
¥4,940,000 (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)
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| 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 |
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| 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.
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| 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
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Report
(4 results)
Research Products
(5 results)
