Abstract
Aim: Reverse cholesterol transport (RCT) is an atheroprotective mechanism in which lipids, especially cholesteryl esters (CE), are transferred from macrophages in the subendothelial space of the arterial wall to the liver for disposal. The terminal RCT step, selective hepatic lipid uptake, is mediated by SR-B1, the HDL receptor, which selectively removes HDL-lipids and releases a protein-rich HDL remnant that in vivo is rapidly relipidated. The relative selectivity decreases with decreasing lipophilicity, CE > triglyceride > phosphatidylcholine. We cite two hypothetical mechanistic models for this process—“gobbling,” i.e., transfer of all HDL-lipids to the cell in a single concerted step, or “nibbling,” multiple cycles of transient SR-B1-HDL association during which one or a few lipid molecules are transferred to the cell. We conducted tests to identify the validity of these two models and whether apo AII, which is more lipophilic than apo AI, was less profoundly excluded from uptake than apo AI.
Published Version
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