Knight B L
MRC Lipoprotein Team, Hammersmith Hospital, London, UK.
Chem Phys Lipids. 1994 Jan;67-68:233-9. doi: 10.1016/0009-3084(94)90142-2.
Three pieces of evidence are presented that suggest that LDL receptors are not greatly involved in the catabolism of intact Lp(a) in vivo. First, studies of normal and heterozygous familial hypercholesterolaemic (FH) siblings who have inherited identical apo(a) alleles have shown that the absence of effective LDL receptors is not invariably associated with an increase in the plasma concentration of Lp(a). Furthermore, in vitro competition studies with reduced Lp(a) from familial-defective apoB subjects indicate that their Lp(a), unlike their LDL, is not enriched with particles containing the binding-defective apoB. Finally, turnover studies in vivo showed no difference in catabolic rate for Lp(a) between normal and FH subjects. There was, however, evidence to suggest that LDL receptors could play a part in the ultimate clearance of Lp(a) by mediating the degradation of its lipid and apoB components after the removal of apo(a) in the circulation.
本文提供了三条证据，表明低密度脂蛋白（LDL）受体在体内完整脂蛋白(a) [Lp(a)] 的分解代谢中作用不大。首先，对继承了相同载脂蛋白(a) [apo(a)] 等位基因的正常和杂合子家族性高胆固醇血症（FH）患者的研究表明，缺乏有效的LDL受体并不总是与血浆Lp(a) 浓度升高相关。此外，来自家族性缺陷载脂蛋白B受试者的还原型Lp(a) 的体外竞争研究表明，他们的Lp(a) 与他们的LDL不同，并不富含含有结合缺陷型载脂蛋白B的颗粒。最后，体内周转研究表明，正常人和FH受试者之间Lp(a) 的分解代谢率没有差异。然而，有证据表明，LDL受体可能通过介导循环中apo(a) 去除后其脂质和载脂蛋白B成分的降解，在Lp(a) 的最终清除中发挥作用。
