The role of preβ-HDL in reverse cholesterol transport, and its plasma concentrations in various disorders

Abstract

Preβ-high-density lipoprotein (HDL) is a minor HDL subfraction with a preβ-electrophoretic mobility. Preβ1-HDL, the smallest preβ-HDL, is the initial acceptor of cell-derived free cholesterol (FC). FC on preβ1-HDL is immediately transferred to preβ2-HDL, and then esterified on preβ3-HDL, the biggest preβ3-HDL, by lecithin: cholesterol acyltransferase (LCAT). Preβ1-HDL decreased during 37°C-incubation by the action of LCAT, but this decrease is completely blocked by a LCAT inhibitor, or anti-human LCAT antibodies. This decrease in preβ1-HDL is also blocked when plasma was incubated with fibroblasts, smooth muscle cells, or macrophages but not with red blood cells.
We recently demonstrated that preβ1-HDL levels increase in coronary artery disease, hypercholesterolemia, and hypertriglyceridemia. Preβ1-HDL levels are also affected by lipid-lowering agents. The relative concentration of preβ1-HDL is normal in CETP deficiency, but the decreasing rate of preβ1-HDL during 37°C-incubation is significantly slower in CETP deficiency than in normal controls. Preβ-HDL/LpA-I ratio is not constant in various disorders, although preβ1-HDL belongs to LpA-I. In summary, preβ-HDL plays an important role in the metabolism of cell-derived cholesterol, and its plasma level changes in various disorders. More study is needed to elucidate the clinical significance of plasma preβ-HDL levels.