Abstract
High density lipoproteins (HDL) display a central role in the processing of plasma cholesterol. While circulating in the vascular space, HDL particles undergo constant remodelling events: for instance, free cholesterol readily exchanges between HDL and other lipoproteins or cell membranes1. Moreover, HDL particles take up most, if not all, of the free cholesterol released from the surface of lipolysed triglyceride-rich lipoproteins (VLDL, chylomicrons,…)2. Such a considerable flux of cholesterol reaching daily the HDL system, can serve as a substrate for the LCAT reaction which, in turn, enhances the efficiency of the cholesterol uptake by HDL3,4. The generated cholesterylesters may be redistributed among plasma low density lipoproteins (VLDL, LDL) by the action of the cholesterol ester transfer protein (CETP) and follow the LDL metabolism5,6. As those sequential activities (free cholesterol uptake, LCAT, CETP) seem to operate in vivo at comparable rates, then HDL would mainly appear as the site of formation of plasma cholesterylesters and of their further redistribution6.
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© 1987 Plenum Press, New York
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Perret, B.P. et al. (1987). Disposal of HDL-Cholesterol to Cultured Granulosa Cells, Endothelial Cells and Hepatocytes: Effects of HDL-Phospholipolysis. In: Malmendier, C.L., Alaupovic, P. (eds) Lipoproteins and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 210. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1268-0_21
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