Triglycerides (TG) are the body’s main source of energy, and a transport system involving lipoprotein particles has evolved to carry them between sites of absorption, biosynthesis, utilisation and storage. A triglyceride molecule typically contains a glycerol backbone and three esterified fatty acids of varying chain length and saturation. Triglycerides are the initial substrate for mitochondrial oxidation of free fatty acids and production of energy as adenosine triphosphate (ATP).

Triglyceride-rich lipoproteins (TRL), ie. very low-density lipoproteins (VLDL) and chylomicrons, are spherical pseudomicellar complexes with a core of TG and cholesteryl esters, and a surface monolayer of phospholipids and free cholesterol, with apolipoproteins stabilising the structure.1,2
Apolipoprotein B (apoB) is the main structural protein in TRL. VLDL are made in the liver and contain full length apoB (apo B-100).1,2 By contrast, chylomicrons are made in the intestine and contain the shorter form, apo B-48.1,2 The key roles of TRL are to transport TG to adipose tissue for storage and to skeletal and cardiac muscle for energy production.2
Remnants are produced during the metabolism of TRL, when they undergo extensive intravascular remodeling. Chylomicrons are metabolised by lipoprotein lipase (LpL) to chylomicron remnants.2 VLDL TG is initially hydrolysed by LpL with formation of VLDL remnants; upon further remodeling by lipases and lipid transfer proteins, intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL) may be formed. Remnant formation may be increased by overproduction of TRL or by genetic or physiological factors that limit lipolysis, or both.2 All chylomicron remnants and variable amounts of VLDL remnants are cleared by the liver.2
References
- Laufs U, Parhofer KG, Ginsberg HN et al. Clinical review on triglycerides. European Heart Journal 2020; 41:99-109
- Ginsberg HN, Packard CJ, Chapman MJ et al. Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies—a consensus statement from the European Atherosclerosis Society. European Heart Journal 2021 Dec 14;42(47):4791-4806.