Cholesterol-rich lipoproteins

Cholesterol-rich lipoprotein particles that carry dietary lipids absorbed in the intestine and deliver them to the liver for uptake. 

Since Lp(a) binds to fibrin, it can be directed to sites of fibrin deposition (vascular injury), providing a high concentration of cholesterol-rich lipoprotein that then can be taken up by macrophages via their scavenger receptors. This... 

Cholesterol-rich lipoproteins of the LDL type are particularly important in the development of arteriosclerosis, in which the arterial walls are altered in connection with an excess plasma cholesterol level. In terms of dietary physiology, it is important that plant foodstuffs are low in cholesterol. By contrast, animal foods can contain large amounts of cholesterol—particularly butter, egg yolk, meat, liver, and brain. 

Mohamed, A. I., A. S. Hussein, S. J. Bhathena, and Y. S. Hafez. The effect of dietary menhaden, olive, and coconut oil fed with three levels of vitamin E on plasma and liver lipids and plasma fatty acid composition in rats. J Nutr Biochem 2002 13(7) 435-441. Kawano, K., S. Qin S, C. Vieu, X. Collet, and X. C. Jiang. Role of hepatic lipase and scavenger receptor BI in clearing phospholipid/free cholesterol-rich lipoproteins in PLTP-deficient... 

The fourth major lipoprotein type, high-density lipoprotein (HDL), originates in the liver and small intestine as small, protein-rich particles that contain relatively little cholesterol and no cholesteryl esters (Fig. 21-40). HDLs contain apoA-I, apoC-I, apoC-II, and other apolipoproteins (Table 21-3), as well as the enzyme lecithin-cholesterol acyl transferase (LCAT), which catalyzes the formation of cholesteryl esters from lecithin (phosphatidylcholine) and cholesterol (Fig. 21-41). LCAT on the surface of nascent (newly forming) HDL particles converts the cholesterol and phosphatidylcholine of chylomicron and VLDL remnants to cholesteryl esters, which begin to form a core, transforming the disk-shaped nascent HDL to a mature, spherical HDL particle. This cholesterol-rich lipoprotein then returns to the liver, where the cholesterol is unloaded some of this cholesterol is converted to bile salts. 

Cholesteryl esters that are internalized via the LDL receptor are hydrolyzed to produce cholesterol and an acyl chain. Cholesterol, in (urn, activates the enzyme acyl-CoA cholesterol acyl-transferase (ACAT) which re-esterifies cholesterol. In an apparently futile cycle, the cholesteryl esters are hydrolyzed by cholesteryl ester hydrolase. The cholesterol moiety has several fates it may leave the cell and bind to an acceptor such as high-density lipoprotein (HDL), it may be converted to steroid hormones, or it may be reesterified by ACAT. When the cellular cholesterol concentration falls, the activity of HMG-CoA reductase is increased, as is the number of LDL receptors, which results in an increase of cellular cholesterol, due both to de novo synthesis and to the uptake of cholesterol-rich lipoproteins in the circulation. An increase in cellular cholesterol results in the rapid decline in the mRNA levels for both HMG-CoA reductase and the LDL receptor. This coordinated regulation is brought about by the presence of an eight nucleotide sequence on the genes which code for both proteins this is termed the sterol regulatory element-1. 

Atherosclerosis and Plasma Lipids - Lipoprotein lipases play a critical role in the metabolism of lipoproteins and thus may be involved in athero-genesis. Hypercholesterolemia in the cholesterol-fed rabbit was attributed to the accumulation of chylomicron remnants, which may be formed on the aorta wall by lipoprotein lipase and deposited in the deep layers of the arterial wall without prior release into the blood stream.13 On this basis, cholesterol-rich lipoproteins in plasma may be the product rather than the cause of the atherogenic process. However, the defect in Type III hyperlipoproteinemia (broad- disease) may be ineffective removal of chylomicron remnant particles from the arterial wall,11 due to a failure of the liver to recognize such particles.15... 

HMGCoA reductase step, which can be inhibited either by cholesterol or phosphorylation of the enzyme, as mediated indirectly by increases in intracellular cAMP. With severe hypercholesterolemia, people may be treated with an HMGCoA reductase inhibitor, such as lovastatin. Cholesterol storage and delivery is controlled by a number of LDL receptors. Low-density lipoprotein is a cholesterol-rich lipoprotein which can deliver cholesterol to many tissues via LDL receptors. As tissue cholesterol levels rise, the importance of cholesterol delivery is less important. When cellular cholesterol levels are high, there is a down-regulation of LDL receptors (a decrease in the number of receptors),... 

Legumes and Their Soluble Fiber Effect on Cholesterol-Rich Lipoproteins... 

Hodis, H.N., Mack, W.J., Azen, S.P., Alaupovic, P., Pogoda, J.M., LaBree, L., Hemphill, L.C., Kramsch, D.M. Blankenhorn, D.H. 1994. Circulation 90 42-49. Triglyceride- and cholesterol-rich lipoproteins have a differential effect on mild/moderate and severe lesion progression as assessed by quantitative coronary angiography in a controlled trial of lovastatin. 

A multitude of genetic defects lead to an increased synthesis and/or a decreased catabolism of cholesterol or LDL. A well characterized although rare defect is the LDL-receptordefect. Ascorbate deficiency unmasks these inherited metabolic defects and leads to an increased plasma concentration of cholesterol-rich lipoproteins, e.g. LDL, and their deposition in the vascular wall. Hypercholesterolemia increases the risk for premature CVD primarily when combined with elevated plasma levels of Lp(a) or triglycerides. 

LDL is cholesterol rich. The production of a cholesterol-rich lipoprotein from a triglyceride-rich lipoprotein occurs by selective removal of triglyceride from VLDL. 

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