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Lipoprotein degradation

Brown, M.S., Basu, S.K., Falck, J.R., Ho, Y.K. and Goldstein, J.C. (1980). The scavenger cell pathway for lipoprotein degradation specificity of the binding site that mediates the uptake of negatively chaiged LDL by macrophages. J. Supramol. Struct. 13, 67-81. [Pg.49]

Carew, T.E., Schwenke, D.C. and Steinberg, O. (1987). Antiatherogenic effect of probucol unrelated to its hyper-cholesterolaemic effect evidence that antioxidants in vim can selectively inhibit low density lipoprotein degradation in macroph -rich fatty streaks slowing the progression of atherosclerosis in the WHHL rabbit. Proc. Natl Acad. Sci. USA 84, 7725-7729. [Pg.49]

A low-density lipoprotein binding in normal (A), co-cuhured (O), and familial hyper-cholesterolemic homozygous (A.) cells. B low density lipoprotein degradation in normal (A), co-cuhured (O), and familial hypercholesterolemic homozygous (A) cells... [Pg.288]

Thyroid hormones regulate the turnover of carbohydrates, lipids, and proteins. They promote glucose absorption, hepatic and renal gluconeogenesis, hepatic glycogenolysis, and glucose utilization in muscle and adipose tissue (18). They increase de novo cholesterol synthesis but increase low-density lipoprotein degradation and cholesterol disposal even more, leading to a net decrease in total and in low-density lipoprotein cholesterol plasma levels (19). Thyroid hormones are anabolic when present at normal concentrations they then stimulate the expression of many key enzymes of metabolism. ... [Pg.1372]

Carew, TJi., Schwenke, D.C., and Steinberg, D. (1987) Antiatherogenic Effect of Probucol Unrelated to Its Hypocholes-terolemic Effect Evidence that Antioxidants In Vivo Can Selectively Inhibit Low Density Lipoprotein Degradation in Macrophage-Rich Fatty Streaks and Slow the Progression of Atherosclerosis in the Watanabe Heritable Hyperlipidemic Rabbits, Proc. Natl. Acad. Sci. USA 84,7725-7729. [Pg.356]

Alaupovic P, Wang CS, McConathy WJ, Weiser D, Downs D (1986). Lipolytic degradation of human very low-density lipoproteins by human milk lipoprotein lipase the identification of lipoprotein B as the main lipoprotein degradation product. Arch Biochem Biophys 244 226-237... [Pg.11]

Lipoproteins in Circulation Are Progressively Degraded by Lipoprotein Lipase... [Pg.842]

FIGURE 25.39 Endocytosis and degradation of lipoprotein particles. (ACAT is acyl-CoA cholesterol acyltransferase.)... [Pg.844]

As an example, the low-density lipoprotein (LDL) molecule and its receptor (Chapter 25) are internalized by means of coated pits containing the LDL receptor. These endocytotic vesicles containing LDL and its receptor fuse to lysosomes in the cell. The receptor is released and recycled back to the cell surface membrane, but the apoprotein of LDL is degraded and the choles-teryl esters metabolized. Synthesis of the LDL receptor is regulated by secondary or tertiary consequences of pinocytosis, eg, by metabolic products—such as choles-... [Pg.430]

Henriksen, T., Mahoney, E.M. and Steinberg, D. (1981). Enhanced macrophage degradation of low density lipoproteins previously incubated with cultured endothelial... [Pg.50]

Esterbauer et al. (1991) have demonstrated that /3-carotene becomes an effective antioxidant after the depletion of vitamin E. Our studies of LDL isolated from matched rheumatoid serum and synovial fluid demonstrate a depletion of /8-carotene (Section 2.2.2.2). Oncley et al. (1952) stated that the progressive changes in the absorption spectra of LDL were correlated with the autooxidation of constituent fatty acids, the auto-oxidation being the most likely cause of carotenoid degradation. The observation that /3-carotene levels in synovial fluid LDL are lower than those of matched plasma LDL (Section 2.2.2) is interesting in that /3-carotene functions as the most effective antioxidant under conditions of low fOi (Burton and Traber, 1990). As discussed above (Section 2.1.3), the rheumatoid joint is both hypoxic and acidotic. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples (Fairburn etal., 1992). This difference could not be accounted for by the lower concentrations of lipids and lipoproteins within synovial fluid. The low levels of both vitamin E and /3-carotene in rheumatoid synovial fluid are consistent with the consumption of lipid-soluble antioxidants within the arthritic joint due to their role in terminating the process of lipid peroxidation (Fairburn et al., 1992). [Pg.106]

Steinbrecher, U.P., Parthasarathy, S., Leake, D.S., Witztum, J.L. and Steinberg, D. (1984). Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids. Proc. Natl Acad. Sci. USA 81, 3883-3887. [Pg.198]

These data suggest that one of possible mechanisms of carotenoid delivery to the neural retina may involve lipoprotein uptake from the basal side of the RPE followed by its retro-endocytosis on the apical site (Lorenzi et al., 2008). Alternatively, the endocytosed lipoprotein may be degraded in the RPE followed by secretion of certain lipophilic components from the lipoprotein at the apical site. Due to low solubility of carotenoids in aqueous solutions, it may be suggested that they are secreted already bound to a protein or that an acceptor protein is available in the interphotoreceptor matrix and/or POS. [Pg.318]

L20. Liu, L, Harpel, P. C., and Gurewich, V., Fibrin-bound lipoprotein(a) promotes plasminogen binding but inhibits fibrin degradation by plasmin. Biochemistry 33, 2554-2560 (1994). [Pg.125]

Snijder, M. L., Polacek, D., Scanu. A. M., and Fless, G. M., Comparative binding and degradation of lipoprotein(a) and low density lipoprotein by human monocyte-derived macrophages. J. Biol. Chem. 267, 339-346 (1992). [Pg.131]

In addition to the common pathways, glycolysis and the TCA cycle, the liver is involved with the pentose phosphate pathway regulation of blood glucose concentration via glycogen turnover and gluconeogenesis interconversion of monosaccharides lipid syntheses lipoprotein formation ketogenesis bile acid and bile salt formation phase I and phase II reactions for detoxification of waste compounds haem synthesis and degradation synthesis of non-essential amino acids and urea synthesis. [Pg.171]

Cholesterol is carried in the bloodstream by hpoproteins such as low density lipoprotein (LDL, or bad cholesterol ) and high density lipoprotein (HDL, good cholesterol ). LDL carries cholesterol from the liver to other parts of the body. LDL attaches to receptors (see Chapter 2) on the cell surface and is taken into the cell interior. It is then degraded and the cholesterol is used as a component for the cell membrane. When there is excessive cholesterol inside the cell, it leads to a reduction in the synthesis of LDL receptors. [Pg.7]


See other pages where Lipoprotein degradation is mentioned: [Pg.34]    [Pg.342]    [Pg.221]    [Pg.133]    [Pg.66]    [Pg.90]    [Pg.377]    [Pg.34]    [Pg.342]    [Pg.221]    [Pg.133]    [Pg.66]    [Pg.90]    [Pg.377]    [Pg.845]    [Pg.225]    [Pg.227]    [Pg.705]    [Pg.100]    [Pg.14]    [Pg.841]    [Pg.179]    [Pg.180]    [Pg.200]    [Pg.442]    [Pg.656]    [Pg.162]    [Pg.105]    [Pg.84]    [Pg.139]    [Pg.237]    [Pg.175]   
See also in sourсe #XX -- [ Pg.276 , Pg.277 , Pg.286 , Pg.288 ]




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