ABSTRACT
High density lipoproteins (HDL) exist in plasma as multiple forms. Populations of HDL that differ in density, composition, electrophoretic mobility and apolipoprotein profile have been identified. These HDL populations differ not only in physicochemical properties but also in their physiological function. Epidemiological studies have provided strong evidence for an inverse relationship between plasma HDL cholesterol levels and coronary heart disease (CHD). The mechanisms by which HDL exerts their antiatherogenic effects have not been conclusively elucidated. However, cell culture studies (Castro & Fielding, 1988; Johnson et al., 1991) and animal models (Rubin et al., 1991; Paszty et al., 1994) have suggested that the antiatherogenic mechanism of HDL involves HDL-mediated removal of cholesterol from cells of the arterial wall and the subsequent transport of cholesterol to the liver for excretion. This process, named reverse cholesterol transport (RCT), limits the accumulation of cholesterol in the arterial wall and is probably responsible for the decreased CHD risk.
