Clinical Pathology: Clinical Chemistry

• Cholesteryl ester transfer protein (CETP) catalyzes the transfer of cholesterol esters to apolipoprotein B (ApoB)-100–containing particles in exchange for triglycerides (TGs). Phospholipid transfer protein (PLTP) facilitates the transfer of phospholipids from other lipoproteins to high-density lipoprotein (HDL), allowing the particle to grow by acquiring surface phospholipid because it also accumulates esterified cholesterol and TG in its core. Once formed, HDL delivers excess lipids, especially cholesterol, to the liver and other tissues.

• HDL is involved in the reverse transport of cholesterol from peripheral tissues to the liver. An important step in this process involves CETP, the plasma protein that facilitates the transfer of cholesteryl esters from HDL to Apoprotein B (ApoB)-100–rich proteins (VLDL and LDL) in exchange for TGs.

• CETP deficiency is an autosomal recessive disorder in which the transfer of cholesterol esters is inhibited. As a result, HDL particles are large and laden with cholesterol ester, and ApoA1 is increased, as are circulating HDL cholesterol levels (typically >100 mg/dL).

• Individuals who are heterozygous for CETP deficiency have moderately increased HDL cholesterol levels.

• Inhibition of CETP is an active area of pharmacologic research given the potential to raise HDL cholesterol levels.

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