Abstract
In humans light (L) LDL is catabolised faster than heavy (H) LDL, of which it is the precursor (Thompson et al., 1982). In familial hypercholesterolaemia (FH) this relationship is lost and the catabolism of L-LDL is decreased more markedly than that of H-LDL. However, the catabolic defect, especially of L-LDL, can be partly reversed by therapeutic measures which stimulate LDL receptors. This suggests that catabolism of L-LDL is normally more dependent on LDL-receptor-mediated mechanisms than is catabolism of H-LDL (Thompson et al., 1984).
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© 1986 Springer-Verlag Berlin Heidelberg
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Kano, M., Koizumi, J., Jadhav, A., Thompson, G.R. (1986). Turnover of Light and Heavy Fractions of Human LDL in Normal and WHHL Rabbits. In: Greten, H., Windler, E., Beisiegel, U. (eds) Receptor-Mediated Uptake in the Liver. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70956-2_12
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DOI: https://doi.org/10.1007/978-3-642-70956-2_12
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