Lipoprotein

any complex or compound containing both lipid and protein

Description
Lipoproteins are important constituents of biological membranes and of myelin. Conjugation with protein facilitates transport of lipids, which are hydrophobic, in the aqueous medium of the plasma. Plasma lipoproteins can be separated by ultracentrifugation, electrophoresis, or immunoelectrophoresis; they migrate electrophoretically with &#945;- and &#946;-globulins, but are usually classified according to their densities (flotation constants). The principal classes by density are chylomicrons, which transport dietary cholesterol and triglycerides from the intestine to the liver and other tissues; very low density lipoproteins (VLDL), which transport triglycerides from intestine and liver to muscle and adipose tissue; low density lipoproteins (LDL), which transport cholesterol to tissues other than the liver; and high density lipoproteins (HDL), which transport cholesterol to the liver for excretion in bile. The protein moiety of a lipoprotein is called an apolipoprotein (or apoprotein). Besides rendering lipids soluble, some apolipoproteins perform biochemical functions such as enzyme activation. The apolipoproteins of plasma lipoproteins are synthesized by the liver and intestinal mucosal cells and vary in molecular weight from 7000 to 500,000. Protein makes up more than 50% of some HDLs but only 1% of chylomicrons. As the proportion of lipid in a lipoprotein increases, its density decreases. A plasma lipoprotein particle is typically spherical, with a hydrophobic core of triacylglycerol, cholesteryl esters, and apolar amino acid residues surrounded by hydrophilic protein structures and phospholipids.

Clinical Relevance
The concentrations of certain serum lipoproteins correlate closely with the risk of atherosclerosis. An HDL cholesterol level below 35 mg/dL (0.90 mmol/L), an LDL cholesterol level above 160 mg/dL (4.15 mmol/L), and a fasting triglyceride level above 250 mg/dL are all independent risk factors for coronary artery disease. Although dietary factors are important in some persons, basal levels of lipoprotein, cholesterol, and triglycerides depend chiefly on heredity. Several phenotypes of familial hyperlipoproteinemia associated with risk of premature cardiovascular disease and death have been identified. See hyperlipoproteinemia. Medical management of patients with coronary artery disease (myocardial infarction, angina pectoris, history of coronary artery bypass graft or coronary angioplasty) and other atherosclerotic disorders (peripheral arterial disease, abdominal aortic aneurysm, carotid artery disease) includes detection and correction of hypercholesterolemia and hyperlipoproteinemia. Reducing elevated LDL cholesterol diminishes the risk of coronary artery disease; besides halting the progression of atherosclerosis, it may even shrink established atherosclerotic lesions. Of persons with elevated LDL cholesterol, 75% can achieve normal levels with diet, weight reduction, and exercise; the remainder need drug treatment. Factors besides familial hyperlipoproteinemias that can elevate LDL cholesterol include diabetes mellitus, hypothyroidism, nephrotic syndrome, obstructive liver disease, and drugs (progestogens, anabolic steroids, corticosteroids, thiazide diuretics). Dietary saturated fat raises LDL cholesterol more than any other dietary component, cholesterol itself not excepted.

See lipoprotein (a)