Abstract
The direct correlation between lipoprotein (a) (Lp(a)) concentrations and atherosclerosis stimulated us to investigate the in vivo interaction of Lp(a) with the liver and the various liver cell types. In untreated rats the serum decay of Lp(a) is comparable to that of LDL. By estrogen treatment the interaction of LDL with parenchymal liver cells is increased 17-fold whereas only a 2-fold effect on Lp(a) is found. The decay of Lp(a) in estrogen-treated rats is slower than for LDL. The data indicate that Lp(a) in vivo shows a less efficient interaction than LDL with the estrogen-induced apo-B,E receptor on parenchymal liver cells. It is suggested that the inability of Lp(a) to interact efficiently with the LDL removal system of the liver might be related to its atherogenic action.
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