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High density lipoproteins roles

Khovidhunkit W, Shigenaga JK, Moser AH, Feingold KR, Grunfeld C. Cholesterol efflux by acute-phase high density lipoprotein Role of lecithin Cholesterol acyltransfer-ase. J Lipid Res 2001 42 967-975. [Pg.103]

Chin et al. (1992) have su ested that oxidized LDL and high-density lipoprotein (HDL) inactivate endothelial cell-derived NO. NO inactivation was due to the oxidized lipids within the lipoprotein particles and was thought to be explained by a chemical reaction between the lipoproteins and NO. Other investigators have shown that relaxation of vascular smooth muscle by acetylcholine or bradykinin (endothelium-dependent vasodilators) is inhibited by LDL (Andrews etal., 1987). The role of NO in the modification of LDL is discussed in full detail in Chapter 2. [Pg.99]

Lorenzi, I, von Eckardstein, A, Cavelier, C, Radosavljevic, S, and Rohrer, L, 2008. Apolipoprotein A-I but not high-density lipoproteins are internalised by RAW macrophages Roles of ATP-binding cassette transporter A1 and scavenger receptor BI. JMolMed 86, 171-183. [Pg.347]

Kwiterovich, P.O. Jr, 1998, The antiatherogenic role of high-density lipoprotein cholesterol. Am. J. Cardiol. 82 13-21. [Pg.146]

One role of high density lipoprotein (HDL) is to collect unesterified cholesterol from cells, including endothelial cells of the artery walls, and return it to the liver where it can not only inhibit cholesterol synthesis but also provide the precursor for bile acid formation. The process is known as reverse cholesterol transfer and its overall effect is to lower the amount of cholesterol in cells and in the blood. Even an excessive intracellular level of cholesterol can be lowered by this reverse transfer process (Figure 22.10). Unfortunately, the level of HDL in the subendothelial space of the arteries is very low, so that this safety valve is not available and all the cholesterol in this space is taken up by the macrophage to form cholesteryl ester. This is then locked within the macrophage (i.e. not available to HDL) and causes damage and then death of the cells, as described above. [Pg.519]

The role of the antioxidant properties of vitamins C, E, and p-carotene in the prevention of cardiovascular disease has been the focus of several recent studies. Antioxidants reduce the oxidation of low-density lipoproteins, which may play a role in the prevention of atherosclerosis. However, an inverse relationship between the intake or plasma levels of these vitamins and the incidence of coronary heart disease has been found in only a few epidemiological studies. One study showed that antioxidants lowered the level of high-density lipoprotein 2 and interfered with the effects of lipid-altering therapies given at the same time. While many groups recommend a varied diet rich in fruits and vegetables for the prevention of coronary artery disease, empirical data do not exist to recommend antioxidant supplementation for the prevention of coronary disease. [Pg.781]

Eckardstein Avon, Huang Y, Assmann G (1994) Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Opin Lipidol 5 404-416... [Pg.545]

While the primary role of LDL appears to be the transport of esterified cholesterol to tissues, the high density lipoproteins (HDL) carry excess cholesterol away from most tissues to the liver 205 207 The apoA-I present in the HDL particle not only binds lipid but activates LCAT, which catalyzes formation of cholesteryl esters which migrate into the interior of the HDL and are carried to the liver. [Pg.1248]

Aviram, M., et al. 1998. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest 101 1581. [Pg.109]

GJ Hopkins, LBF Chang, PJ Barter. Role of lipid transfers in the formation of a subpopulation of small high density lipoproteins. J Lipid Res 26 218-229, 1985. [Pg.374]

M28. Marcel, Y. L., Vezina, C., Emond, D., and Suzue, G., Heterogeneity of human high density lipoproteins Presence of lipoproteins with and without apoE and their roles as substrates for lecithin cholesterol acyltransferase reaction. Proc. Natl. Acad. Sci. U.S.A. 77, 2969-2973 (1980). [Pg.286]

R17, Rose, H. G., and Juliano, J., Regulation of plasma lecithimcholesterol acyltransferase in man. III. Role of high density lipoprotein cholesteryl esters in the activating effect of a high-fat test meal. J. Lipid Res. 20, 399-407 (1979). [Pg.291]

Von Eckardstein, A., Nofer, J.R., and Assmann, G., 2001, High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport, Arterioscler. Thromb. Vase. Biol. 21 13-27. [Pg.150]

These lipids are insoluble in water and are classified on the basis of their ultracentrifugal properties into chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) in order of ascending density. Table 2.4 gives the classification and roles of lipoproteins. [Pg.35]

Cholesterol and triacylglycerols are transported in body fluids in the form of lipoprotein particles. Each particle consists of a core of hydrophobic lipids surrounded by a shell of more polar lipids and apoproteins. The protein components of these macromolecular aggregates have two roles they solubilize hydrophobic lipids and contain cell-targeting signals. Lipoprotein particles are classified according to increasing density (Table 26.1) chylomicrons, chylomicron remnants, very low density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). Ten principal apoproteins have been isolated and characterized. They are synthesized and secreted by the liver and the intestine. [Pg.1078]

Weng, W., and Bieslow, J. L. (1996). Dramatically increased high-density-lipoprotein cholesterol, increased remnant clearance, and insulin hypersensitivity in apolipopiotein A-II knockout mice suggest a complex role for apolipoprotein A-IJ in atherosclerosis susceptibility. Proc. Nati. Acad. Sci. U.S.A. 93,14788-14794. [Pg.376]


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See also in sourсe #XX -- [ Pg.85 ]




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