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lipoprotein

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Lipoprotein

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.

lipoprotein

[‚lip·ə′prō‚tēn]
(biochemistry)
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.
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References in periodicals archive
Endogeneous pathway: the liver assembles triglycerides and cholesterol on apo B100 in very low- density lipoprotein (VLDL) during fasting, with recycling of remnants.
The increase in HDL, triglyceride, and VLDL levels, with a statistically significant difference in VLDL between the three groups, is similar to that observed by HOENIG et al.
Table III.- Effect of various diets on (TPC), (VLDL), (LDL), (HDL) and triglycerides of dietary induced hypercholesterolemic rats on pre-treatment and post-treatment.
VLDL (mg/l) HDL(mg/l) LDL (mg/l) E1 90.26 [+ or -] 4.7 (c) 95.41 [+ or -] 3.3 (c) E2 211 [+ or -] 3.7 (a) 201.66 [+ or -] 2.9 (a) E3 120 [+ or -] 5.6 (bd) 111 [+ or -] 2.2 (bd) E4 99 [+ or -] 4.6 (bd) 99.8 [+ or -] 2.8 (bd) E5 92 [+ or -] 4.5.5 (c) 94.91 [+ or -] 3.1 (c) VLDL (mg/l) Total cholesterol mg/l TG (mg/l) E1 24 [+ or -] 1,8 (c) 51.02 [+ or -] 1.3 (c) E2 50 [+ or -] 2.1 (a) 41.18 [+ or -] 1.8 (a) E3 31.25 [+ or -] 1.8 (bd) 50.12 [+ or -] 1.6 (bd) E4 27.12 [+ or -] 2 (bd) 49.79 [+ or -] 1.4 (bd) E5 251 [+ or -] 1.8 (c) 51.31 [+ or -] 1.7 (c) VLDL (mg/l) Groups E1 25.05 [+ or -] 1.8 (c) E2 73.62 [+ or -] 2.1 (a) E3 56.53 [+ or -] 1.9 (bd) E4 61.78 [+ or -] 2.4 (bd) E5 18.85 [+ or -] 1.1 (c) E1: control group, E2: High Fructose, E3: High Fructose + T.
Multivariate analysis showed an association between elevated VLDL levels and blood pressure (BP) with SCD patients being more liable to developing diastolic dysfunction (depicted here by elevated DBP) which ultimately increases mortality [31].
The relative hormones and VLDL concentration in plasma were determined, and the results are shown in Figure 1.
11649 (fosfotungstato 0,4mmol/L y cloruro de magnesio 20 mmol/L), que se mezclo con 0.2 mL de la muestra de suero, se agito bien y se dejo durante 10 minutos a temperatura ambiente; se centrifugo por 15 minutos a 4000 rpm en el equipo Thermo: en el precipitado quedaron las VLDL, IDL y LDL, y en el sobrenadante quedaron las HDL.
Increased VLDL could increase LDLC while also resulting in modulation of particle size.
Acute and chronic exposure to ethanol in embryonic stages significantly (P<0.05) increses plasma concentration of VLDL cholesterol in newborn hatching chick (figure 5).
These alterations also followed suppression of VLDL particle maturation and secretion from liver, decrease the VLDL level in plasma, and further decrease the LDL level and AI value [31].
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