食中和脂肪的超脂性影响通过PGC-1β SREBP的同活性介导
Jiandie Lin1, Ruojing Yang, Paul T Tarr
1Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Cell
|February 1, 2005
概括
高脂肪饮食增加肝脏PGC-1β和SREBP的表达,促进高脂血症. PGC-1β减少肝脏脂肪,但增加血脂,有助于动脉动脉生成.
科学领域:
- 代谢和分子生物学
- 心血管研究研究心血管研究
背景情况:
- PGC-1联合激活剂调节转录因子和核受体.
- 类固醇响应元素结合蛋白 (SREBPs) 控制肝脏中的脂原基因.
研究的目的:
- 调查PGC-1β在高脂肪饮食引起的高脂血症和动脉动脉生成中的作用.
- 阐明PGC-1β影响肝脂代谢和脂蛋白运输的机制.
主要方法:
- 在高脂肪养后,对肝脏基因表达 (PGC-1beta,SREBP1c,SREBP1a) 的分析.
- 评估PGC-1β对SREBP的同激活及其在脂质基因表达中的作用.
- 评估PGC-1beta对肝脏脂肪积累和循环脂质水平的影响.
- 研究PGC-1beta与肝脏X受体α (LXRalpha) 的相互作用.
主要成果:
- 高脂肪食在肝脏中调节了PGC-1β和SREBP1c/1a.
- PGC-1β协同激活SREBPs,刺激脂原基因表达,对SREBP介导作用至关重要.
- PGC-1beta降低了肝脏脂肪的积累,但增加了循环中的甘油三和VLDL胆固醇.
- PGC-1β 同激活了LXRalpha,增强了脂蛋白的运输.
结论:
- PGC-1beta在肝脂代谢中起着双重作用,减少肝脂肪,同时促进高脂血症.
- 食中的和脂肪可以通过PGC-1β和SREBP激活诱导高脂血症和动脉动脉生成.
- PGC-1β对LXRalpha的同激活有助于改变脂蛋白代谢.
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