SR-B1 belongs to the class B scavenger receptor, or CD36 super family. SR-B1 and CD36 share an affinity for a wide array of ligands. Although they exhibit similar ligand binding specificity, SR-B1 and CD36 have some very specific lipid transport functions. Whereas SR-B1 primarily facilitates the selective delivery of cholesteryl esters (CEs) and cholesterol from HDL particles to the liver and non-placental steroidogenic tissues, as well as participating in cholesterol efflux from cells, CD36 primarily mediates the uptake of long-chain fatty acids in high fatty acid-requiring organs such as the heart, skeletal muscle and adipose tissue. However, CD36 also mediates cholesterol efflux and facilitates selective lipoprotein-CE delivery, although less efficiently than SR-B1. Interestingly, the ability or efficiency of SR-B1 to mediate fatty acid uptake has not been reported. In this paper, using overexpression and siRNA-mediated knockdown of SR-B1, we show that SR-B1 possesses the ability to facilitate fatty acid uptake. Moreover, this function is not blocked by BLT-1, a specific chemical inhibitor of HDL-CE uptake activity of SR-B1, nor by sulfo-N-succinimidyl oleate, which inhibits fatty acid uptake by CD36. Attenuated fatty acid uptake was also observed in primary adipocytes isolated from SR-B1 knockout mice. In conclusion, facilitation of fatty acid uptake is an additional function that is mediated by SR-B1.

中文翻译：

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B型清道夫受体1促进细胞脂肪酸的摄取。

SR-B1属于B类清除剂受体，或CD36超家族。SR-B1和CD36对多种配体具有亲和力。尽管它们表现出相似的配体结合特异性，但SR-B1和CD36具有一些非常特殊的脂质转运功能。SR-B1主要促进HDL颗粒向肝脏和非胎盘类固醇生成组织选择性递送胆固醇酯（CEs）和胆固醇，并参与细胞的胆固醇外流，而CD36主要介导长链脂肪的摄取需要高脂肪酸的器官（例如心脏，骨骼肌和脂肪组织）中的脂肪酸。然而，尽管CD36的效率不如SR-B1，但它也可介导胆固醇外流并促进选择性脂蛋白-CE的递送。有趣的是，尚未报道SR-B1介导脂肪酸摄取的能力或效率。在本文中，利用SR-B1的过表达和siRNA介导的敲低，我们证明SR-B1具有促进脂肪酸摄取的能力。此外，该功能不会被SR-B1的HDL-CE摄取活性的特异性化学抑制剂BLT-1所阻断，也不会被抑制CD36吸收脂肪酸的磺基N-琥珀酰亚胺基油酸酯所阻断。在分离自SR-B1基因敲除小鼠的原代脂肪细胞中也观察到脂肪酸吸收减弱。总之，促进脂肪酸摄入是SR-B1介导的另一功能。SR-B1的HDL-CE摄取活性的特定化学抑制剂，也不能被磺基-N-琥珀酰亚胺基油酸酯抑制CD36摄取脂肪酸。在分离自SR-B1基因敲除小鼠的原代脂肪细胞中也观察到脂肪酸吸收减弱。总之，促进脂肪酸摄入是SR-B1介导的另一功能。SR-B1的HDL-CE摄取活性的特定化学抑制剂，也不能被磺基-N-琥珀酰亚胺基油酸酯抑制CD36摄取脂肪酸。在分离自SR-B1基因敲除小鼠的原代脂肪细胞中也观察到脂肪酸吸收减弱。总之，促进脂肪酸摄入是SR-B1介导的另一功能。