Lipoprotein Metabolism: Structure and Function


Lipoproteins are particles in plasma which carry cholesterol and triglyceride. Lipoprotein metabolism is described based on structure and function of their apolipoproteins and the enzymes, transfer proteins and receptors involved in their assembly and catabolism. Genetic defects in lipoprotein metabolism highlight the functions of these metabolic parameters.

Keywords: cholesterol; triglyceride; lipoprotein; atherosclerosis; dyslipidaemia

Figure 1.

(a) Structure of a lipoprotein particle with triglyceride (TG) and cholesteryl ester (CE) core and phospholipid, cholesterol and protein surface. (b) Size and buoyancy characteristics of lipoproteins. CE, cholesteryl ester; LDL, low‐density lipoprotein; TG, triglyceride; VLDL, very low‐density lipoprotein. Lipoproteins can be characterized by lipid and protein content, by size or by density.

Figure 2.

Defects in very low‐density lipoprotein (VLDL) secretion. CE, cholesteryl ester; TG, triglyceride. Compared to normal VLDLs, large VLDLs are secreted in familial hypertriglyceridaemia and small VLDLs are secreted in familial combined hyperlipidaemia.

Figure 3.

Lipoprotein lipase‐mediated triglyceride removal. Lipoprotein lipase on the blood vessel luminal surface hydrolyses TG in the lipoprotein core. Free fatty acids are taken up by the fat cell and re‐esterified to adipocyte TG for storage. CE, cholesteryl ester; FFA, free fatty acid; LPL, lipoprotein lipase; TG, triglyceride.

Figure 4.

Pathophysiology of remnant removal disease. Two defects in lipoprotein metabolism are required: an increase in lipoprotein secretion into plasma and a defect in apoE. CE, cholesteryl ester; LDL, low‐density lipoprotein; TG, triglyceride; VLDL, very low‐density lipoprotein.

Figure 5.

Physiology of LDL catabolism. LDL can be taken on by the LDL receptor in the liver or peripheral tissues. Modified LDL may be directed towards scavenger receptors in macrophages. CE, cholesteryl ester; LDL, low‐density lipoprotein; TG, triglyceride.

Figure 6.

Physiology of high‐density lipoproteins (HDL). Nascent LDL arises from the liver and intestine. Cholesterol and phospholipids are provided to HDL by surface material from processed VLDL. The cholesterol is esterified by LCAT and the maturation of HDL begins. LCAT, lecithin cholesterol acyltransferase.


Further Reading

Current Opinion in Lipidology. [Journal published six times per year with extensive reviews].

Scriver CR, Beaudet AL, Valle D et al. (2002) The Metabolic and Molecular Bases of Inherited Disease, 8th edn, chaps 114–123. New York: McGraw‐Hill.

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Brunzell, John D, and Chait, Alan(May 2003) Lipoprotein Metabolism: Structure and Function. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0000609]