The saturable uptake and degradation of 125I-labelled human very low density lipoproteins in cultured rat liver endothelial cells could be effectively inhibited by high density lipoproteins (HDL) from normal subjects. Up to eight times more HDL (in relation to cholesterol content) was needed from patients with hyperlipoproteinaemia (HLP) type III to give the same inhibition. The HDL apolipoprotein (apo) E concentrations that were needed to give the same inhibition as normal HDL apo E were between 3 and 50 times higher in HLP type III. Our results suggest that the lipoprotein abnormality in HLP type III not only affects chylomicron remnant metabolism but also the composition and function of HDL.
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