Plasma Lipoprotein Phenotype in Response to Cholesteryl Ester Transfer Protein Levels in Dyslipoproteinemia

There are two mamallian systems for reverse cholesterol transport, one of which is dependent on the presence of cholesteryl ester transfer protein (CETP) activity1,2. The rat is typical of species lacking CETP activity and under these conditions, triglyceride-rich lipoproteins and their remnants transport only that cholesterol which was initially associated with the nascent particles. Rat HDL on the other hand, is rich in apoE and transports cholesterol derived from both splanchnic and peripheral organs, and esterified by LCAT and eventually returns it to the liver, via an apoE receptor. In contrast in the human system, the high CETP activity promotes the transfer of 2/3 or more of cholesteryl esters in HDL to the triglyceride-rich lipoproteins and their remnants. These recipient jparticles are then actively removed by hepatic apoE and apoB/E receptors3. In individuals with active receptors, this represents the major pathway for reverse cholesterol transport while a minority of HDL cholesterol is cleared directly by an apoE-mediated pathway. Direct selective uptake of HDL cholesteryl esters by the liver has also been suggested, but recent evidence indicated that this route is also apoE-mediated4.