Hepatic retention and elimination of cholesteryl linoleyl ether after injection of labeled acetylated LDL or chylomicrons.

Rat mesenteric duct chylomicrons labeled with [3H]cholesteryl linoleyl ether and human acetylated low density lipoproteins labeled with [14C]cholesteryl linoleyl ether were injected simultaneously into rats. 3 h after injection 80-90% of the injected radioactivity were recovered in the liver and the ratio of 3H/14C in the liver was the same as in the injected material. The 3H/14C ratio declined gradually over a period of 18 days due to loss of [3H]cholesteryl ether which had been injected with the chylomicrons, and retention of the same compound injected bound to acetylated LDL. The loss from the liver of the chylomicron-bound cholesteryl linoleyl ether was shown to occur through the bile, and its elimination from the body was verified by monitoring fecal excretion. The present results provide evidence that hepatic persistence of a nonhydrolyzable analog of cholesteryl ester is a function of the cell type which has ingested the lipid. Thus, the uptake of labeled chylomicrons by hepatocytes results in a slow but progressive excretion of the nonhydrolyzable lipid through the bile, while the preferential uptake of acetylated LDL by nonparenchymal cells of liver and by the spleen leads to persistence of the lipid in the organ.