Analysis of the paternal transmission of obesity.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K07194
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Genome biology
• Research Institution: Gunma 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
• Keywords: 肥満 / 父性遺伝 / インプリンティング

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.

Free Research Field

分子生物学

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