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Triacylglycerol-rich lipoproteins

VAN DEN BERG H and VAN VLIET T (1998) Effects of simultaneous, single oral doses of 3-carotene, with lutein or lycopene on the (3-carotene and retinyl ester responses in the triacylglycerol-rich lipoprotein fractions in men. Am J Clin Nutr 68(1) 82-89. [Pg.126]

M. E. O Neill and D. I. Thumham, Intestinal absorption of beta-carotene, lycopene and lutein in men and women following a standard meal Response curves in the triacylglycerol-rich lipoprotein fraction, Br. J. Nutr. 79 (1998) 149-159. [Pg.378]

Hu X, Jandacek RJ and White WS. 2000. Intestinal absortion of (3-carotene ingested with a meal rich in sunflower oil or beef tallow postprandial appearance in triacylglycerol-rich lipoproteins in women. Am J Clin Nutr 71 1170-1180. [Pg.215]

Engelmann B., Streich S., SchonthierU. M., Richter W. O., and Duhm J. (1992). Changes of membrane phospholipid composition of human erythrocytes in hyperlipidemias. I. Increased phosphatidylcholine and reduced sphingomyelin in patients with elevated levels of triacylglycerol-rich lipoproteins. Biochim. Biophys. Acta Lipids Lipid Metab. 1165 32-37. [Pg.230]

Redgrave, T. G., Rakic, V., Mortimer, B.-C., and Mamo, J. C. L. (1992), Effects of sphingomyelin and phosphatidylcholine acyl chains on the clearance of triacylglycerol-rich lipoproteins from plasma. Studies with lipid emulsions in rats, Biochim. Biophys. Acta, 1126, 65-72. [Pg.1358]

It has been suggested that Pgp plays a role in the transport of prcnyleystcin-rue thy 1 esters or cholesterol (58). In addition, esterification of cholesterol and triacylglycerol-rich lipoprotein secretion was inhibited by inhibitors of Pgp (59), whereas cholesterol seemed to be transported by Pgp also (60). [Pg.637]

Jackson RL, Tajima S, Yamamura T, Yokoyama S, Yamamoto A. Comparison of apolipoprotein C-II-deftcient triacylglycerol-rich lipoproteins and trioleoyiglycerol/phosphatidylcholine-stabilized particles as substrates for lipoprotein lipase. Biochim BiophysActa 1986 875 211-19. [Pg.973]

All mammalian triacylglycerol-rich lipoproteins contain apoB that has been shown to be an obligatory factor for their formation and degradation." From the clinical point of view, mnch interest has focused on apoB becanse elevated levels of the apoB-containing lipoproteins have been shown to have a central role in the development of the most common circulatory disease in the indnstrialized world, atherosclerosis." ... [Pg.160]

Fig. 4. Model showing the interactions between the endothelial cell surface, triacylglycerol-rich lipoproteins, apo C2, and lipoprotein lipase (LPL). Two LPL molecules are shown reacting with the same VLDL particle. These are representative of the multiple LPLs that probably react with each triacylglycerol-rich lipoprotein. The location of the recently identified glycosylphosphatidylinositol-anchored HDL binding protein-1 within the substrate-lipase complex has not yet been identified. Fig. 4. Model showing the interactions between the endothelial cell surface, triacylglycerol-rich lipoproteins, apo C2, and lipoprotein lipase (LPL). Two LPL molecules are shown reacting with the same VLDL particle. These are representative of the multiple LPLs that probably react with each triacylglycerol-rich lipoprotein. The location of the recently identified glycosylphosphatidylinositol-anchored HDL binding protein-1 within the substrate-lipase complex has not yet been identified.
Fig. 5. Mechanism of remnant lipoprotein formation at the endothelial surface. Apo B is not illustrated. FFA, unesterified fatty acid MG, monoacylglycerol closed triangles, apo C2 closed circles, apo E. This model reflects the appearance of partially lipolyzed lipoprotein particles in the circulation during lipoprotein lipase-mediated lipolysis of triacylglycerol-rich lipoproteins. Fig. 5. Mechanism of remnant lipoprotein formation at the endothelial surface. Apo B is not illustrated. FFA, unesterified fatty acid MG, monoacylglycerol closed triangles, apo C2 closed circles, apo E. This model reflects the appearance of partially lipolyzed lipoprotein particles in the circulation during lipoprotein lipase-mediated lipolysis of triacylglycerol-rich lipoproteins.
Removal of triacylglycerol-rich lipoproteins from the plasma. 565... [Pg.555]

In the following sections, our still incomplete knowledge about the events involved in receptor-mediated plasma clearance of triacylglycerol-rich lipoproteins is outlined. [Pg.565]

While these recent studies indicate the requirement for non-receptor-mediated steps in the overall clearance pathways for triacylglycerol-rich lipoproteins, the ultimate uptake occurs by endocytotic mechanisms involving specific receptors. Studies in a variety of experimental systems predicted that the removal of chylomicron remnants occurs independent of the LDL receptor, despite the presence of apo E on these particles. Accordingly, individuals with homozygous FH, who lack functional LDL receptors, show no signs of delayed clearance of chylomicron remnants. [Pg.566]

Zambon, A., S. Bertocco, N. Vitturi, V. Polentarutti, D. Viancello, and G. Crepaldi. 2003. Relevance of hepatic lipase to the metabolism of triacylglycerol-rich lipoproteins. Biochemical Society Transactions 31 1070-1074. [Pg.199]

Elevated levels of lipoprotein-associated cholesterol in the blood, particularly that associated with LDL but also that in the more triacylglycerol-rich lipoproteins, are associated with the formation of cholesterol-rich atheromatous plaque in the vessel wall, eventually leading to diffuse atherosclerotic vascular disease resulting in acute cardiovascular events, such as a myocardial infarction, a stroke, or symptomatic peripheral vascular insufficiency. High levels of HDL in the blood, therefore, are believed to be vasculoprotective, because these high levels increase the rate of reverse cholesterol transport away from the blood vessels and toward the liver ( out of harm s way ). [Pg.635]

Investigators have shown that a decrease in the release of tissue plasminogen activator (tPA) and an elevation of plasminogen activator inhibitor 1 (PAI-1) will reduce fibrinolytic function. It has emerged that triacylglycerol-rich lipoproteins stimulate PAI-1 secretion from endothelial cells, and furthermore it has been shown that OxLDL induces secretion, whereas native LDL has no detectable... [Pg.166]

Unlike triacylglycerol-rich lipoproteins, nascent HDL have not been identified within subcellular compartments. Much of our knowledge is obtained from observations of nascent HDL in liver perfusates. At this early stage, they are disc-shaped rather than spherical and consist of a bilayer of mainly phosphatidylcholine with apoAi and apoE at the margins of the disc. Similar particles are also found in intestinal lymph. After excretion into the plasma, HDL acquire additional surface components phospholipids, cholesterol and apoproteins by transfer from chylomicrons and VLDL... [Pg.205]

The most studied lipoproteins have been the HDL and, to a lesser extent, the LDL because they have a more specific and tightly organized structure than the triacylglycerol-rich lipoproteins. HDL has a readily soluble apolipoprotein component and model studies of the interaction of these peptides with phospholipid and neutral lipid mixtures have been invaluable. In contrast, the insolubility of the LDL apoproteins has restricted progress in the study of their structure. [Pg.216]


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See also in sourсe #XX -- [ Pg.534 , Pg.537 , Pg.538 , Pg.539 , Pg.540 , Pg.541 , Pg.542 , Pg.543 ]




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