Lp(a) catabolism in hypercholesterolaemic individuals.
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.
Knight
B L
BL
MRC Lipoprotein Team, Hammersmith Hospital, London, UK.
D000483:Alleles; D001053:Apolipoproteins / Q000235:genetics / Q000378:metabolism; D001055:Apolipoproteins B / Q000235:genetics / Q000378:metabolism; D053241:Apoprotein(a); D001667:Binding, Competitive; D005260:Female; D006579:Heterozygote; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D066298:In Vitro Techniques; D017270:Lipoprotein(a) / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D009154:Mutation; D010375:Pedigree; D011973:Receptors, LDL / Q000378:metabolism
D001053:Apolipoproteins; D001055:Apolipoproteins B; D017270:Lipoprotein(a); D008077:Lipoproteins, LDL; D011973:Receptors, LDL; D053241:Apoprotein(a)