As chylomicrons circulate in the body, they acquire molecules of apolipoproteins C and E, and through interaction with endothelial lipases can lose a large fraction of their triacylglycerol. These changes convert them to chylomicron remnants which bind to LDL receptors, primarily on the surfaces of liver cells, clearing them from the circulation. This whole sequence of events is rapid: the normal lifespan of a chylomicron is 30 - 60 minutes (Redgrave 2004).
As they circulate, VLDL are acted on by lipoprotein lipases on the endothelial surfaces of blood vessels, liberating fatty acids and glycerol to be taken up by tissues and converting the VLDL first to intermediate density lipoproteins (IDL) and then to low density lipoproteins (LDL) (Gibbons et al. 2004).
HDL remodeling includes the conversion of HDL-associated cholesterol to cholesterol esters (remodeling of spherical HDL), the transfer of HDL lipids to target cells with the regeneration of pre-beta HDL (lipid-poor apoA-I), and the conversion of pre-beta HDL to discoidal HDL (Rye et al. 1999).