Data now available suggest that a dynamic equilibrium exists in the plasma lipoproteins. Chylomicrons and very low density lipoproteins (VLDL) are primary secretory products of cells and carry triglycerides through the blood stream. As intravascular triglyceride hydrolysis occurs via the action of lipoprotein lipase (LPL), the further metabolism of nontriglyceride constituents of chylomicrons and VLDL can be followed along two interrelated pathways. Along the core pathway, cholesterol ester increasingly becomes a major core lipid with resultant formation of intermediate density (IDL, or remnant particles) and eventually low density (LDL) lipoprotein. Concomitant with reduction of core volume, redundant surface lipids and proteins move along a surface pathway and either form high density (HDL) lipoprotein precursors, or become associated with existing HDL particles. Cholesterol esters are formed via the action of lecithin: cholesterol acyltransferase (LCAT) in HDL. Therefore, action of LPL and LCAT on triglyceride-rich lipoproteins and their catabolic products is sufficient and necessary for formation, in plasma, of LDL and HDL. Once formed, all plasma lipoproteins are further remodelled by the activity of exchange and transfer reactions. In humans, a major remodelling occurs through exchange of LDL and HDL cholesterol ester by VLDL (and chylomicrons) triglyceride. The reaction is the main source of cholesterol esters in triglyceride-rich lipoproteins and is responsible for the enrichment of LDL and HDL with triglycerides. When followed by triglyceride lipolysis, this cycle results in limitation of size and cholesterol content of both LDL and HDL. The physiology and pathophysiology of the plasma lipid transport system in humans can therefore be fully appreciated only when the interrelations of all these metabolic reactions is taken into account.