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FTO对能源需求的影响与食物摄入量相比
1Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen AB24 2TZ, Scotland, UK. j.speakman@abdn.ac.uk
Nature
|April 3, 2010
概括
这种FTO基因变体rs9939609与肥胖有关. 虽然人类研究表明对食物摄入的影响,但FTO缺乏的小鼠的新陈代谢率增加,表明复杂的肥胖机制.
科学领域:
- 遗传学和肥胖研究研究
- 代谢调节研究 研究 代谢调节研究
背景情况:
- 脂肪质量和肥胖相关基因 (FTO) 附近的内基单核酸多态 (SNP) rs9939609是首个与体重指数 (BMI) 相关的已识别的常见变异.
- 以前的人类研究将rs9939609与食物摄入量和腹感的改变联系在一起,但与能量消耗不一致.
- 菲舍尔等人. 菲舍尔等人. 最近创建的Fto-无活化小鼠 (Fto(-/-)) 证明了对肥胖的保护.
研究的目的:
- 研究人类肥胖FTO基因与小鼠Fto基因功能的对比机制.
- 探索FTO在物种之间代谢率和食物摄入调节中的作用.
主要方法:
- 对SNP rs9939609现有的人类遗传关联研究及其与食物摄入,和和能量消耗的关系的分析.
- 对菲舍尔等人研究结果的回顾. 在Fto(-/-) 小鼠身上,与野生类型的 littermates相比,重点关注食物摄入量和代谢率.
主要成果:
- 人类研究将FTO SNP rs9939609与食物摄入量和腹感的变化联系起来,但对能量消耗没有一致的影响.
- Fto(-/-) 鼠在食物摄入量上没有显著差异,但其代谢率较高,这表明通过增加能量消耗来预防肥胖.
- 在小鼠中观察到的效应在机理上与FTO SNP在人类研究中建议的效应相反.
结论:
- 人类FTO基因变异和小鼠Fto基因功能的对比作用需要进一步研究.
- 内体SNP rs9939609对肥胖的影响可能涉及复杂的,特定于物种的调节机制,影响新陈代谢.
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