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Cholesterol feeding

A6, B24, M17). Cholesterol feeding is known to increase apo-B100 and LDL concentrations considerably apparently without changing Lp(a) and apo(a) levels. Only diets enriched in fish oils have been reported to lower plasma Lp(a) concentrations (D7, G25, H10, M23, N4), probably as result of a reduced apo-Blon synthesis and therefore reduced hepatic Lp(a) synthesis. [Pg.91]

The thiolase and HMG-CoA synthase exhibit some regulatory properties in rat liver (cholesterol feeding causes a decrease in these enzyme activities in the cytosol but not in the mitochondria). However, the primary regulation of cholesterol biosynthesis appears to be centered on the HMG-CoA reductase reaction. HMG-CoA reductase is found on the endoplasmic reticulum, has a molecular weight of 97,092, and consists of 887 amino acids in a single polypeptide chain. The sequence of the enzyme was deduced by Michael Brown and Joseph Goldstein from the sequence of a piece of complimentary DNA (cDNA) derived from mRNA that codes for the reductase. The enzyme... [Pg.462]

Malinow, M.R., McLaughlin, P., Naito, H.K., Lewis, L.A., and McNulty, W.P. 1978. Effect of alfalfa meal on shrinkage (regression) of atherosclerotic plaques during cholesterol feeding in monkeys. [Pg.200]

Vuoristo, M. and Miettinen, T.A. 1994. Absorption, metabolism, and serum concentrations of cholesterol in vegetarians Effects of cholesterol feeding. Am. J. Clin. Nutr. 59, 1325-1331. [Pg.203]

ApoE-containing HDL, obtained by heparin-Sepharose affinity chromatography, contains apoA-I, apoA-II, and apoC, as well as apoE (W12, W18). Clearance frou. the plasm, appears to be dependent on a specific hepatic receptor for apoE, which binds apoE-containing HDL and chylomicron remnants, but not other lipoproteins (H35, Mil, S28). Canine apoE-HDLC, with apoE as the only detectable apoprotein, is cleared from the plasma very rapidly by the liver (more than 90% in the first 20 minutes after intravenous injection) (M15). In adult man, dogs, and swine the apoE receptor numbers do not seem to be significantly reduced by cholesterol feeding (H35, Mil). [Pg.250]

ApoB-100,E receptors present in the liver of immature dogs and swine are suppressed by cholesterol feeding and are not apparently active in the liver of mature animals (H35, Mil). The hepatic apoB-100,E receptors are thought to be identical to the apoB-100 receptors demonstrated in many extrahepatic cell types (B21). ApoE-containing HDL in vitro have a 20- to 25-fold greater affinity for apoB-100, E receptors than LDL (16, P15) it seems, because there are four receptor binding sites for each molecule of HDLC as opposed to one binding site for LDL (P15, P16). [Pg.250]

M17. Mahley, R. W., Weisgraber, K. H., and Innerarity, T., Atherogenic hyperlipoproteinemia induced by cholesterol feeding in the Patas monkey. Biochemistry 15, 2979-2985 (1976). [Pg.285]

Hodis, H.N., Crawford, D.W., Sevanian, A. 1991. Cholesterol feeding increases plasma and aortic tissue cholesterol oxide levels in parallel further evidence for the role of cholesterol oxidation in artherosclerosis. Artherosclerosis 89, 117-126. [Pg.433]

PURPOSE AND RATIONALE Rabbits are known to be susceptible to hypercholesterolemia and arteriosclerosis after excessive cholesterol feeding (supplemented with 0.3-2% cholesterol in the diet). Therefore, this approach has been chosen by many authors to study the effect of potential anti-atherosclerotic drags. For studying the atherogenic potential of a candidate compound a low cholesterol concentration in the diet (0.1-0.3%) is recommended (pro-atherogenic). [Pg.187]

Cockerels (Tennent et al. 1960) and turkeys (Simpson and Harms 1969) are very susceptible to cholesterol feeding and develop marked hypercholesterolemia in rather short periods. Atherosclerosis could also be induced in cockerels by high doses of oestrogen without atherogenic diet (Caldwell and Suy-dam 1959). [Pg.187]

Ming-Peng et al. (1990) studied high density lipoproteins and prevention of experimental atherosclerosis in tree shrews (Tupaia belangera yunalis). In contrast to rabbits, no increased lipid deposition in aortic intima after cholesterol feeding was found in tree shrews. [Pg.188]

Male Sprague Dawley or spontaneously hypertensive stroke prone Wistar or Lewis rats with adjuvant induced arthritis weighing 150-300 g or New Zealand rabbits with arteriosclerosis induced by cholesterol feeding for 3 months are used. The animals receive the test compound by oral, intravenous, intraperitoneal, or subcutaneous administration. Control animals are treated with vehicle alone. Prior to thrombus induction, the animals are pretreated by s.c. injection of... [Pg.288]

Cholesterol feeding. Mice were divided into four groups, two of which were fed a normal diet and two of which were fed a cholesterol-rich diet. HMG-CoA reductase mRNA and protein from liver were then isolated and quantified. Graph A shows the results of the mRNA isolation. [Pg.1100]

There is experimental evidence that suggests that some oxysterols, but not pure cholesterol, are the prime cause of atherosclerotic lesion formation (162). Upon cholesterol feeding, a strong relationship was seen between plasma oxysterols and aortic wall oxysterols. One may speculate that the deposition of pure lipids, such as cholesterol and its esters, may be merely a secondary process in response to oxysterol-induced endothelial cell injury. Cell injury/dysfunction and the subsequent disruption of endothelial barrier function by oxysterols (163, 164) could initiate the early events in atherosclerosis. Such injury could allow increased uptake... [Pg.633]

In another study, 24 healthy, normal-weight men with normal cholesterol levels were fed diets that contained 300 mg or 800 mg of cholesterol per day in ten-day periods, and in a 21-day period, less than 50 mg per day of cholesterol. Subsequently, 8 g, 16 g, or 25 g of olestra were added to each of the diets in ten-day periods. The diets were of the typical American variety and contained approximately 20% of their calories as protein, 40% as carbohydrates, and 40% as fat. Care was taken so that there were no significant reductions in weight. Adding olestra to the diet lowered both total and LDL cholesterol at all levels of cholesterol feeding (57). [Pg.1878]

Duymelinck C, Dauwe SE, Nouwen EJ, De Broe ME, Verpooten GA. Cholesterol feeding accentuates the cyclosporine-induced elevation of renal plasminogen activator inhibitor type 1. Kidney Int 1997 51 1818-1830. [Pg.659]

The answer is d. (Murray, pp 258-297. Scriver, pp 2705-2716. Sack, pp 121-138. Wilson, pp 362-367.) Regulation of cholesterol metabolism is by definition exerted at the committed and rate-controlling step. This is the reaction catalyzed by 3-hydroxy-3-methylglutaryl CoA reductase. Reductase activity is reduced by fasting and by cholesterol feeding and thus provides effective feedback control of cholesterol metabolism. The statin class of drugs act at this site. [Pg.223]

Cholesterol 7a-hydroxyIase has been partially purified from rat and rabbit liver (H5). The enzyme is located in the smooth endoplasmic reticulum and is dependent on cytochrome F-450 and NADPH-cytochrome P-450 reductase for activity (H5). The particular cytochrome P-450 associated with microsomal cholesterol 7a-hydroxylase activity constitutes a small fraction of total liver cytochrome P-450 and, in the rabbit, it appears to be a subfraction of cytochrome P-450lm4 (B28). Measurement of the activity of this enzyme by isotope incorporation is complicated by dilution of added cholesterol by endogenous microsomal cholesterol. A method has now been developed to remove cholesterol fit>m microsomes, so that the mass of 7a-hydroxycholesterol formed during enzyme assay can be accurately calculated (S25). Using this assay, cholic acid feeding was shown to suppress the activity of cholesterol 7a-hydroxylase in rat liver, whereas cholesterol feeding did not (S25). [Pg.179]

Figure 1. Effect of nifedipine on the extent of aortic lesions (planimetry of sudano-philic lesions) induced by cholesterol feeding. Key (n = 13) , placebo and [3,... Figure 1. Effect of nifedipine on the extent of aortic lesions (planimetry of sudano-philic lesions) induced by cholesterol feeding. Key (n = 13) , placebo and [3,...
Gnerre, C., Schuster, G. U., Roth, A., Handschin, C., Johansson, L., Looser, R., Parini, P., Podvinec, M., Robertsson, K., Gustafsson, J. A., et al. (2005) LXR deficiency and cholesterol feeding affect the expression and phenobarbital-mediated induction of cytochromes P450 in mouse liver. J. Lipid Res. 46, 1633-1642. [Pg.317]

On the basis of the data reviewed in this chapter, it seems likely that there are functionally distinct pools of cholesterol in the intestinal epithelial cell that serve different metabolic functions. These pools are illustrated diagrammatically in the model of an epithelial cell shown in Fig. 14. Pool A is defined as having been derived largely from the uptake of luminal unesterified cholesterol (arrow 1) and serves as a major substrate for the CoA-dependent esterification reaction (arrow 2). The cholesterol esters that result from this reaction are incorporated into the hydro-phobic core of the chylomicron particle. Following cholesterol feeding there is a marked increase in apparent ACAT activity in the intestinal epithelium that seems to be related to an increase in the amount of intracellular cholesterol available to the enzyme under the in vitro conditions of the assay rather than to an increase in the... [Pg.144]

Pools A and B also appear to be functionally distinct with respect to the role of the sterol in these pools to effectively regulate the rate of cholesterol synthesis within the intestinal epithehal cell. For example, cholesterol feeding in the rat and in man... [Pg.145]


See other pages where Cholesterol feeding is mentioned: [Pg.135]    [Pg.249]    [Pg.252]    [Pg.274]    [Pg.285]    [Pg.285]    [Pg.286]    [Pg.291]    [Pg.329]    [Pg.273]    [Pg.1100]    [Pg.559]    [Pg.560]    [Pg.218]    [Pg.262]    [Pg.759]    [Pg.210]    [Pg.6]    [Pg.129]    [Pg.139]    [Pg.165]    [Pg.238]    [Pg.239]   


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