Upon entry into the circulation, chylomicrons (containing apo B-48) produced by the small intestine, and VLDL (containing apo B-100) produced by the liver undergo LPL–mediated lipolysis mainly in peripheral tissues, notably adipose tissue and muscle. Intravascular remodelling of TRL equally involves the actions of lipid transfer proteins (CETP, PLTP) and additional lipases (HL and EL) with the formation of remnant particles. TRL remnants are typically enriched in cholesterol and apo E, but depleted in triglyceride; they are principally catabolized in the liver upon uptake through the LRP and LDL receptor pathways. TRL remnants can contribute either directly to plaque formation following penetration of the arterial wall at sites of enhanced endothelial permeability,21 or potentially indirectly following liberation of lipolytic products (such as FFA and lysolecithin) which may activate pro-inflammatory signalling pathways in endothelial cells.20,21 Abbreviations: apo, apolipoprotein; CETP, cholesteryl ester transfer protein; EL, endothelial lipase; FFA, free fatty acids; HL, hepatic lipase; LDL, low-density lipoprotein; LPL, lipoprotein lipase; LRP, lipoprotein receptor-related protein; PLTP, phospholipid transfer protein; TRL, triglyceride-rich lipoprotein; VLDL, very-low density lipoprotein.