Abstract
It has been suggested that apoE may play a central role in reverse cholesterol transport in rats. By this hypothesis, cholesteryl esters (CE) accumulate in high density lipoprotein (HDL) particles, which acquire apoE at the expense of apoA-I, and the apoE targets them for rapid hepatic uptake. However, the pathway has not been directly assessed in vivo. We directly traced the metabolism of HDL1 cholesteryl esters in rats. To do this, rat HDL1 was labeled in its apoE and CE moieties, and HDL2 free of apoE was labeled in its apoA-I and CE moieties; 14C- or 3H-labeled cholesteryl-oleyl ether traced the CE moieties and the 125I- or 131I-labeled N-methyltyramine cellobiose (NMTC) ligand traced the apolipoprotein moieties. The labeled HDLs were injected, plasma decays were followed, and tissues were examined after 24 h. ApoE tracer decayed from plasma 2.4-times faster than HDL1 CE and 1.8-times faster than HDL2 CE. HDL1 CE decayed significantly more slowly than HDL2 CE (0.75-times). As expected, hepatic uptake of HDL2 CE was mostly by selective (indirect) uptake. However, hepatic uptake of HDL1 CE was at a fractional rate significantly lower than that of HDL2 CE (0.69-times), even though the uptake of apoE was much higher. The plasma decay of HDL1 apoE evidently reflects in large part the uptake of apoE after transfer to other fractions, and it over-estimates the clearance of HDL1 CE. Selective uptake plays the major role in hepatic HDL CE uptake in rats.
Highlights
It has been suggested that apoE may play a central role in reverse cholesterol transport in rats
Associated studies showed that the apoA-I uptake by liver closely measured uptake of the holo-high density lipoprotein (HDL), excluding the possibility that hepatic selective uptake might represent the endocytotic uptake of HDL particles depleted of apoA-I tracer and enriched in unlabeled apoE [10, 17, 26]
Direct interpretation of these earlier data would indicate that in rats only about one-third of hepatic HDL cholesteryl esters (CE) uptake is by uptake of HDL particles, including uptake both with or without the benefit of apoE
Summary
It has been suggested that apoE may play a central role in reverse cholesterol transport in rats. By this hypothesis, cholesteryl esters (CE) accumulate in high density lipoprotein (HDL) particles, which acquire apoE at the expense of apoA-I, and the apoE targets them for rapid hepatic uptake. ApoE tracer decayed from plasma 2.4-timesfaster than HDLl CE and 1.8-times faster than HDLp CE. HDLl CE decayed significantly more slowly than HDL, CE (0.75-times).As expected, hepatic uptake of HDL, CE was mostly by selective (indirect)uptake. Hepatic uptake of HDLl CE was at a fractional rate significantly lower than that of HDLZ CE (0.69-times),even though the uptake of apoE was much higher. Role of HDL, in cholesteryl ester uptake in rats.J Lipid Res. 1993. 34: 571-579
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