Cholesterol

Lipoproteins

Lipoproteins are macromolecular aggregates of lipids and apolipoproteins, varying in their proportions of component molecules and the type of proteins present. There are four types of lipoprotein. Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) are cholesterol-rich types, whereas chylomicrons and very low-density lipoproteins (VLDL) are triglyceride-rich types.

Cholesterol-rich lipoproteins:
LDL particles are the main carriers of cholesterol and the principal lipoproteins involved in atherosclerosis. They account for 60-70% of plasma cholesterol, so the concentration of LDL-C provides a good estimate of the total concentration of serum cholesterol.^1,2 It has been shown that small dense LDL particles are the most atherogenic. They are absorbed by macrophages within the arterial wall to form lipid-rich foam cells, the initial stage in the pathogenesis of atherosclerotic plaques.¹

HDL particles are the smallest, but most abundant of the lipoproteins, and contain almost a quarter of serum cholesterol. They do not cause atherosclerosis, but actually protect against its development. This is because they return about 20-30% of cholesterol from peripheral tissue through the blood to the liver for excretion.^1,2

Triglyceride-rich lipoproteins:
Chylomicrons are the largest in size, lowest in density and are not associated with atherosclerosis. They transport dietary triglyceride from the intestine to the sites of use and storage, and are cleared rapidly from the bloodstream.^1,2

VLDL particles are similar in structure to chylomicrons but smaller. They are the main carriers of endogenous (liver-synthesised) triglycerides and cholesterol from the liver to sites of use or storage. As triglycerides are removed, the VLDL remnants continue to circulate as LDL particles, so can play a part in atherosclerosis development.^1,2

References:
1. In: Fast Facts - Hyperlipidaemia. Eds Durrington P, Sniderman A. Health Press Ltd, Oxford, 2000. 1-17.
2. In: Manual of Lipid Disorders, 2nd Edition. Eds Gotto A, Pownall H. Williams & Wilkins, US, 1999. 2-10.