Uptake and cellular degradation of low-density lipoprotein.

Abstract

In vitro data suggest that low-density lipoprotein (LDL) is bound to specific receptors located in pits on the surface of fibroblasts by a high-affinity process and subsequently undergoes catabolism in lysosomes. This binding seems to be mediated by ionic interaction between LDL and its receptor, the latter being totally or partially absent from the fibroblasts of patients with familial hypercholesterolaemia (FH). In vivo data suggest that LDL is also catabolised by a concentration-dependent, low-affinity pathway which is probably mainly located in the liver. LDL catabolism is reduced in FH and after saturated fat feeding, whereas polyunsaturated fat has the reverse effect. Hypocatabolism of LDL alters LDL composition, accelerates atherosclerosis and may lead to premature death from coronary heart disease.