脂肪组织ATP结合盒载体A1有助于高密度脂蛋白生物发生 in vivo
Soonkyu Chung1, Janet K Sawyer, Abraham K Gebre
1Department of Pathology/Section on Lipid Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Circulation
|September 21, 2011
概括
脂肪组织ATP结合盒载体A1 (ABCA1) 对于高密度脂蛋白 (HDL) 生成至关重要. 在小鼠中删除它会通过损害新生的HDL颗粒形成来降低HDL胆固醇.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 脂质代谢 脂质代谢是什么
背景情况:
- 脂肪组织是主要的自由胆固醇储存库.
- ATP结合盒载体A1 (ABCA1) 对于高密度脂蛋白 (HDL) 生物发生至关重要.
- 在体内脂肪组织ABCA1在HDL生产中的作用尚不清楚.
研究的目的:
- 为了研究脂肪组织ABCA1对HDL生物发生的体内贡献.
- 阐明脂肪细胞特异性ABCA1删除对胆固醇稳态和高密度胆固醇代谢的影响.
主要方法:
- 产生脂肪细胞特异性的ABCA1淘汰小鼠 (ABCA1(-A/-A)).
- 测量血的HDL胆固醇和阿波脂蛋白AI水平.
- 评估自由胆固醇含量和胆固醇从脂肪组织流出.
- 分析新生的高密度LH粒子形成和高密度LH标记物吸收.
主要成果:
- 脂肪细胞ABCA1删除显著降低了血的HDL胆固醇和阿波利波蛋白AI.
- 缺乏ABCA1的脂肪组织显示,自由胆固醇增加,对阿波利波蛋白AI的流量受损.
- 脂肪组织的ABCA1缺陷减少了新生的HDL颗粒的形成,特别是更大的HDL颗粒.
- 胆固醇流向现有的高密度胆固醇和高密度胆固醇标记物代谢不受脂肪细胞ABCA1删除的影响.
结论:
- 脂肪组织ABCA1-依赖的胆固醇排放对于系统性HDL生物发生是必不可少的.
- 脂肪组织ABCA1在脂肪细胞胆固醇恒温中发挥着至关重要的作用.
- 由于脂肪细胞ABCA1缺乏,新生的HDL颗粒形成的减少降低了血HDL度.
相关概念视频
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