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lipoprotein (lĭpˌəprōˈtēn), any organic compound that is composed of both protein and the various fatty substances classed as lipids, including fatty acids and steroids such as cholesterol. The lipoprotein complex of proteins and steroids is usually provided by a weak, noncovalent interaction; proteins complexed with some other lipids do so by the information of covalent chemical bonds. There are several types of lipoproteins present in human blood, including low-density lipoproteins (LDLs)—molecules with a larger molecular weight and a relatively low percentage of protein—and high-density lipoproteins (HDLs)—molecules with a smaller molecular weight and a relatively high percentage of protein. LDLs are the main transport for cholesterol through the body. HDLs appear to carry excess cholesterol to the liver for processing. Studies have found that high levels of HDLs, which seem to retard or even reverse the formation of cholesterol plaque in the arteries (see arteriosclerosis), reduce the risk of cardiovascular disease. Cell membranes are essentially lipoprotein in nature; the membrane is a continuous sheet of lipid molecules, largely phospholipids, in close association with proteins that either face one side of the membrane or penetrate all the way through the membrane.
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Classes of conjugated proteins consisting of a protein combined with a lipid. The normal functioning of higher organisms requires movement of insoluble lipids, such as cholesterol, steroid hormones, bile, and triglycerides, between tissues. To accomplish this movement, lipids are incorporated into macromolecular complexes called lipoproteins.

All major types of lipoproteins share a general structure. The core of these spherical particles contains primarily cholesteryl ester and triglyceride. These insoluble molecules are surrounded by a coating of proteins and phospholipids that are amphipathic; that is, they have both polar and nonpolar regions. Lipoproteins vary by size and density. The largest lipoproteins, chylomicrons, are up to 500 nanometers in diameter, and since they contain primarily triglyceride they are so buoyant that they float in plasma. Very low density lipoproteins (VLDL) also primarily transport triglyceride. Low-density lipoproteins (LDL) and the smallest, most dense lipoproteins, high-density lipoproteins (HDL), transport cholesterol. The interactions of these particles with cell surface receptors and with metabolic enzymes are mediated by the protein components of the particles, termed apolipoproteins. See Cholesterol, Triglyceride

Chylomicrons contain triglyceride (fat) from the diet. In addition, they carry fat-soluble vitamins, such as vitamin A and E, into the circulation. Chylomicrons are produced in the intestine, enter the body via the lymphatic system, and then enter the bloodstream.

Very low density lipoproteins are made in the liver and contain triglyceride that is synthesized either from excess carbohydrate sources of calories or from fatty acids that enter the liver and are reassembled into triglyceride. Lipoprotein lipase (LpL) is an enzyme found on the surface of blood vessels that is responsible for the breakdown of triglyceride in lipoproteins. The partially degraded lipoproteins are termed remnants. They are ultimately removed from the circulation by the liver.

Low-density lipoproteins result after triglyceride is removed from very low density lipoproteins. This leaves a smaller, denser particle that primarily contains cholesteryl ester as its core lipid and a single protein called apoB. Cells throughout the body contain an LDL receptor that recognizes apoB. This allows the uptake of low-density lipoproteins into cells, supplying them with cholesterol. When sufficient low-density lipoproteins and cholesterol are available, cells use them in preference to synthesizing new cholesterol from precursors. In contrast, high-density lipoproteins both deliver and remove cholesterol from tissues.

Blood levels of lipoproteins are major factors regulating risk for development of coronary artery atherosclerosis. Via unknown mechanisms, low-density lipoproteins and remnant lipoproteins infiltrate and then become attached to extracellular matrix molecules within the artery. Some of the lipoproteins are internalized by macrophages and smooth muscle cells. This might first require chemical modification such as oxidation of the lipids. The resulting pathological findings are deposition of cholesterol in cells and matrix within the vessel wall, leading to a decrease in the diameter of the artery.

In contrast, high-density lipoproteins appear to prevent atherosclerosis formation. The reasons are not entirely understood. Most likely, high-density lipoproteins remove excess cholesterol that accumulates in the artery, or prevent the oxidation of low-density lipoproteins. See Arteriosclerosis

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.


Any of a class of conjugated proteins consisting of a protein combined with a lipid.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Familial lipoprotein lipase deficiency and other causes of the chylomicronemia syndrome.
AMT has developed Glybera as a treatment for patients with the genetic disorder lipoprotein lipase deficiency.
Indeed, the rare autosomal recessive deficiency of apo C2 can lead to a decrease in lipoprotein lipase deficiency as profound as that in familial lipoprotein lipase deficiency (34, 35).
AMT has developed Glybera as a treatment for patients with the genetic disorder lipoprotein lipase deficiency. The dossier for Glybera that was submitted to the European Medicines Agency (EMA) is in the process of being submitted for re-evaluation.
Heterozygous lipoprotein lipase deficiency due to a missense mutation as the cause of impaired triglyceride tolerance with multiple lipoprotein abnormalities.
Human gene therapy company Amsterdam Molecular Therapeutics (AMT) (Euronext:AMT) today released data showing that its gene therapy Glybera (alipogene tiparvovec) significantly reduces the risk of pancreatitis in patients with Lipoprotein Lipase Deficiency (LPLD).
Glybera is a gene therapy product under development for the treatment of lipoprotein lipase deficiency (LPLD) that is currently under review for marketing approval with the European Medicines Agency (EMA).
Amsterdam Molecular Therapeutics (AMT)(Euronext:AMT), a human gene therapy company, announced on Friday the receipt of an opinion on its Marketing Authorisation Application (MAA) for Glybera (alipogene tiparvovec) as a potential therapy for Lipoprotein Lipase Deficiency (LPLD).
23 November 2010 - Dutch Amsterdam Molecular Therapeutics (AMS: AMT) said today it has submitted its responses to the Day 120 questions posed by the European Medicines Agency (EMA) as part of the review process for Glybera, a gene therapy for lipoprotein lipase deficiency (LPLD).
This diagnostic tool rapidly diagnoses patients with complete and partial lipoprotein lipase deficiency (LPLD).

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