第28节 哈普洛因不足引发双稳定性表观遗传肥胖
Kevin Dalgaard1, Kathrin Landgraf2, Steffen Heyne1
1Max Planck Institute of Immunobiology and Epigenetics, Stübeweg 51, 79108 Freiburg, Germany.
Cell
|January 30, 2016
概括
研究人员发现了一种依赖Trim28的基因网络, 这一发现揭示了一种新的肥胖遗传机制,
科学领域:
- 遗传学
- 发育生物学
- 代谢疾病
背景情况:
- 肥胖影响全球50多亿人, 传统的孟德尔遗传学仍然无法解释.
- 了解肥胖的遗传基础对于开发有效的干预措施至关重要.
研究的目的:
- 确定参与肥胖遗传的新型遗传网络.
- 研究Trim28在调节体重和基因表达中的作用.
- 在小鼠和人类的肥胖中探索多的潜力.
主要方法:
- 使用Trim28 ((+/D9) 突变小鼠研究体重分布和基因表达.
- 在肥胖和正常小鼠中分析了印记基因网络 (Nnat,Peg3,Cdkn1c,Plagl1) 的表达.
- 在人类儿童中进行脂肪组织转录组分析.
主要成果:
- 突变小鼠Trim28(+/D9) 呈现双模体重量分布,表明一个随机肥胖表型.
- 肥胖状态与特定印记基因的表达减少相关.
- 根据Trim28表达和印记基因失调,人类儿童表现出不同的子群体,反映出小鼠表型.
结论:
- 发现了一个依赖Trim28的网络,
- 在小鼠和人类的肥胖中提供了离散多的证据.
- 突出了复杂的特征遗传学,进化和医学的影响.
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