Triglycerides are transported by the largest and most lipid-rich of the lipoprotein particles, namely, chylomicrons and very low density lipoproteins (VLDL). These particles are buoyant because of the high triglyceride content, which makes up approximately 90% by weight of the chylomicron and 70% by weight of the VLDL.

The chylomicron transports exogenous or dietary fat and cholesterol, whereas VLDL transports endogenous triglyceride and cholesterol in lipoproteins synthesized and secreted by the liver. Both chylomicrons and VLDL are hydrolyzed at the capillary surface by the enzyme lipoprotein lipase. Lipoprotein lipase catalyzes the hydrolysis of triglyceride in the lipid core of these particles, producing smaller particles known as remnants. We currently believe the remnants are atherogenic and that this is one reason why hypertriglyceridemia may predispose to coronary artery disease.

Chylomicron remnants are recognized and removed by hepatic receptors that contain apolipoprotein (apo) E. The rate of clearance of remnant particles depends on which subfraction of apo E is present. Particles containing apo EII are removed more slowly than those with apo EIII and EIV.

The dietary cholesterol from the chylomicron remnant particles is thought to down-regulate the hepatic low-density lipoprotein (LDL) receptors. VLDL remnants, also called intermediate-density lipoprotein (IDL), contain apo E and may be removed by the liver through the LDL or B/E receptor. The decrease in activity of these receptors results in apparent oversynthesis of LDL, the end-product of VLDL and IDL metabolism.

LDL is the major cholesterol carrier, followed by high-density lipoprotein (HDL). LDL carries approximately up to three-fourths of the cholesterol in the Mood, and about two-thirds of LDL is removed by specific LDL receptors as it circulates. The other portion is removed by low-affinity pathways. HDL contains approximately 50% cholesterol and phospholipid. HDL is synthesized in the liver, the intestine and also originates from the surface of chylomicrons and VLDL during lipolysis. HDL acquires cholesterol from peripheral tissues and is esterified by the lecithin cholesterol acyltransferase or LCAT to cholesteryl ester. The cholesteryl ester may then be transferred from HDL to LDL, IDL or VLDL by the cholesteryl ester transfer protein. Thus, cholesterol can be transported to the liver indirectly by HDL, and HDL fractions containing apo E may directly transport HDL to the liver. HDL exists in a nascent form before being converted into spherical particles. There is some evidence that apo AI may play a particularly important role in this reverse cholesterol transport process.

HDL may be subdivided in several ways: one based on its apoprotein content and one based on its density (e.g., HDL₂ and HDL₃). In hypertriglyceridemia, the formation of HDL from the hydrolysis of triglyceride-rich particles may be diminished. In addition, when postprandial lipemia occurs, or when there is a prolonged elevation of triglyceride-rich lipoproteins, an increased transfer of triglyceride from triglyceride-rich lipoprotein particles into LDL and HDL may occur in exchange for cholesteryl ester. The metabolic changes associated with hypertriglyceridemia may decrease the concentration of HDL and result in small, dense particles of LDL and HDL.