Selective uptake of cholesteryl esters from low density lipoproteins in vitro and in vivo
1991
SR Green | RC Pittman
Evidence for the direct uptake (“selective uptake”) of cholesteryl esters (CE) from low density lipoproteins (LDL) by perfused luteinized rat ovaries (Azhar, S., A. Cooper, L. Tsai, W. Maffe, and E. Reaven. 1988. J. Lipid Res. 29: 869-882) led to this examination of LDL selective uptake in cultured cells and in rats using LDL doubly labeled with intracellularly trapped tracers of the CE and apoB moieties. Studies in vitro demonstrated LDL selective uptake by human fibroblasts at a low rate relative to LDL particle uptake; the fractional rate of this selective uptake increased with decreasing LDL particle size. Mouse Y1-BS1 adrenal cortical tumor cells also selectively took up LDL CE; on ACTH treatment, LDL selective uptake increased in parallel with high density lipoproteins (HDL) selective uptake, and accounted for the majority of LDL CE uptake. Metabolism of doubly labeled LDL was examined in rats. Adrenal gland and liver selectively took up CE from rat LDL, as did lung and adipose tissue. Selective uptake from human LDL was at a lower fractional rate than from rat LDL, and could not be demonstrated in as many organs. Although selective uptake from LDL by ovaries of adult rats was not significant, ovaries of immature rats consistently exhibited LDL selective uptake; on treatment of these rats with hormones to produce superovulated, luteinized ovaries, LDL selective uptake increased in the ovaries and nowhere else. Selective uptake was also apparent in liver, where it accounted for 27% of total hepatic uptake of rat LDL CE. These studies indicate a significant contribution of selective uptake to LDL CE metabolism in rats, suggesting the possibility of a role in other animals as well.
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