Abstract
The presence in human plasma of a protein that promotes bidirectional transfers of neutral lipids (cholesteryl esters and triglycerides) between all lipoprotein particles was first reported in 1978 (1, 2). This protein was identified as cholesteryl ester transfer protein (CETP) and subsequently cloned in 1987 by Drayna et al. (3). CETP promotes the equilibration of cholesteryl esters and triglycerides between HDL, LDL, and triglyceride-rich lipoproteins (TRL), which include VLDL that are produced in the liver, intestinally-derived chylomicrons, and chylomicron remnants. As most of the cholesteryl esters in plasma originate in HDL in the reaction catalyzed by lecithin:cholesterol acyltransferase, and triglycerides mostly enter the plasma compartment as a component of TRL, this process of equilibration results in a net mass transfer of cholesteryl esters from potentially anti-atherogenic HDL particles to LDL and TRL, which are known to be atherogenic.
Highlights
The presence in human plasma of a protein that promotes bidirectional transfers of neutral lipids between all lipoprotein particles was first reported in 1978 [1, 2]
Subsequent studies of Taq1 B polymorphisms of the cholesteryl ester transfer protein (CETP) gene provided the first indication of an inverse relationship between CETP gene expression and activity and plasma HDL-cholesterol levels [4]
This raised the possibility that inhibition of CETP activity may increase the concentration of HDL, thereby reducing cardiovascular risk, This relationship is supported by a recent meta-analysis of 92 studies involving 113,833 participants, which concluded that people carrying CETP gene polymorphisms that are associated with decreased CETP activity and mass have elevated HDL-cholesterol levels and are at decreased risk of having a coronary event [5]
Summary
The presence in human plasma of a protein that promotes bidirectional transfers of neutral lipids (cholesteryl esters and triglycerides) between all lipoprotein particles was first reported in 1978 [1, 2]. Subsequent studies of Taq1 B polymorphisms of the CETP gene provided the first indication of an inverse relationship between CETP gene expression and activity and plasma HDL-cholesterol levels [4]. These individuals had reduced apoB and LDL levels, which was attributed to increased catabolism of apoBcontaining lipoproteins [9].
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