Human blood monocyte-derived macrophages that had been cultured in medium containing human serum for 7 days degraded the abnormal very-low-density lipoproteins (VLDL) from the plasma of subjects with type III hyperlipoproteinaemia by two distinct saturable processes. One process was stimulated when cells from normal subjects were preincubated with lipoprotein-free medium, was inhibited by excess unlabelled low-density lipoproteins (LDL) and was absent from cells from subjects with homozygous familial hypercholesterolaemia; on these criteria it was identified as an LDL-receptor-dependent process. Degradation by the second process was of equal magnitude in both cell types and was unaffected by excess unlabelled LDL or acetylated LDL. The activity of this process was reduced when the cells were preincubated in lipoprotein-free medium. The abnormal VLDL from the plasma of cholesterol-fed rabbits were also degraded by this process, which was similar to that in mouse peritoneal macrophages mediated by the receptor for VLDL of beta-electrophoretic mobility [Goldstein, Ho, Brown, Innerarity & Mahley (1980) J. Biol. Chem. 255, 1839-1848].

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