高密度脂蛋白胆固醇的脂肪细胞调节
YuZhen Zhang1, Fiona C McGillicuddy, Christine C Hinkle
1Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6160, USA.
Circulation
|March 10, 2010
概括
脂肪细胞通过ABCA1和SR-BI载体促进胆固醇转移到HDL. 这种新功能可能会在2型糖尿病等炎症性脂肪性疾病中受损.
科学领域:
- 代谢研究的研究.
- 脂质代谢 脂质代谢 是一种
- 脂肪细胞生物学 脂肪细胞生物学
背景情况:
- 脂肪组织储存大量的自由胆固醇.
- 脂肪组织在高密度脂蛋白 (HDL) 胆固醇脂化中的作用在体内尚未得到充分证实.
研究的目的:
- 在体内和体外研究脂肪细胞在胆固醇转移到HDL中的作用.
- 为了确定参与这个过程的特定胆固醇运输体.
主要方法:
- 使用野生型和淘汰型脂肪细胞 (ABCA1,SR-BI,ABCG1) 进行胆固醇外流检测.
- 在体内研究涉及向小鼠注射标记脂肪细胞的腹膜内注射.
- 评估瘤亡因子-阿尔法对输送体表达和胆固醇流动的影响.
主要成果:
- 胆固醇流向阿波利波蛋白A-I (apoA-I) 和HDL3分别在ABCA1(-/-) 和SR-BI(-/-) 脂肪细胞中受损.
- 在体内研究证实了脂肪细胞对高密度胆固醇的贡献,这取决于apoA-I水平.
- 瘤亡因子-α降低了ABCA1和SR-BI的表达,损害了胆固醇排泄.
结论:
- 脂肪细胞在促进胆固醇在体内转移到高密度胆固醇方面具有新的代谢功能.
- 脂肪细胞SR-BI和ABCA1,但不是ABCG1,参与了这种胆固醇转移过程.
- 在炎症性脂肪性疾病 (如2型糖尿病) 中,HDL的脂肪细胞调节可能会受到损害.
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