| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effect of leisure time exercise on high-density lipoprotein cholesterol, its subclasses, and size in Asian Indians Bhalodkar, N. C., S. Blum, et al. (2005), Am J Cardiol 96(1): 98-100. Abstract: Asian Indians have a greater prevalence and incidence of coronary artery disease than other ethnic groups, despite similar routine lipid profiles. High-density lipoprotein (HDL) cholesterol, particularly the large subclass, is predominantly associated with coronary artery disease protection. Exercise reduces coronary artery disease risk by improving HDL cholesterol levels. The effect of exercise on HDL cholesterol concentrations, subclasses, and size, measured by nuclear magnetic resonance spectroscopy, was assessed in 388 healthy Asian Indians. Exercise was associated with significantly greater concentrations of total HDL cholesterol, entirely due to significant increases in the cardioprotective large HDL subclass and larger HDL cholesterol particle sizes. |
| Effect of lifibrol on the metabolism of low density lipoproteins and cholesterol Vega, G. L., K. von Bergmann, et al. (1999), J Intern Med 246(1): 1-9. Abstract: Lifibrol is a powerful cholesterol-lowering drug of unknown mechanism of action. This investigation was carried out to determine whether the major action of lifibrol is to enhance clearance of low density lipoproteins (LDL) through the LDL-receptor pathway, and if so, whether the drug exerts its action by altering the excretion of bile acids (acidic steroids), the absorption of cholesterol, or the synthesis of cholesterol. In a first study, in two patients with complete absence of LDL receptors, lifibrol therapy had essentially no effect on plasma LDL concentrations; in two others who had a marked reduction in LDL-receptor activity, response to the drug was attenuated. These findings suggest that lifibrol requires an intact LDL-receptor pathway to exert its action. In a second study, in patients with primary moderate hypercholesterolemia, isotope kinetic studies showed that lifibrol enhanced the fractional catabolic rate of LDL-apolipoprotein B (apo B), but had no effect on transport rates of LDL; these observations likewise support the probability that lifibrol acts mainly to increase the activity of the LDL-receptor pathway. However, in a third study in hypercholesterolemic patients, lifibrol therapy failed to increase acidic steroid excretion, inhibit cholesterol absorption, or reduce net cholesterol balance. Furthermore, lifibrol treatment did not significantly reduce urinary excretion of mevalonic acid. In contrast, in a parallel study, simvastatin therapy, which is known to inhibit cholesterol synthesis, gave the expected decrease in net cholesterol balance and reduction in urinary excretion of mevalonic acid. Thus, lifibrol, like statins, appears to increase the activity of LDL receptors; but in contrast to findings with statins, it was not possible to detect a significant decreased synthesis of cholesterol, either from balance studies or from urinary excretion of mevalonic acid. This finding raises the possibility that lifibrol activates the LDL-receptor pathway through a different mechanisms which remains to be determined. |
| Effect of lindane on mitochondrial side-chain cleavage of cholesterol in mice Sircar, S. and P. Lahiri (1990), Toxicology 61(1): 41-6. Abstract: Cholesterol side-chain cleavage of mitochondria, the key rate limiting step in steroid biosynthesis in ovarian tissues, was studied in female Swiss mice fed lindane (gamma-hexachlorocyclohexane) at various doses and over varying periods. The insecticide adversely affected cholesterol side-chain cleavage of the ovary as judged by decreased conversion of this sterol to pregnenolone and subsequently to progesterone in a dose-dependent manner. The formation of pregnenolone was maximally inhibited (75% inhibition) at the highest intake of insecticide with simultaneous inhibition of its conversion to progesterone. At all doses, the rate of inhibition of pregnenolone formation was comparatively higher than its conversion to progesterone. The significant inhibition of cholesterol side-chain cleavage by lindane and resultant decrease in the rate of steroidogenesis in the ovary would account for the observed gonadal hormone deficiency and related reproductive disorders in the lindane-fed mice. |
| Effect of linseed oil on fatty acid composition of low- and very low density lipoproteins, cholesterol and its fractions in the blood serum of albino rats Kaminskas, A., D. A. Mikalauskaite, et al. (1991), Vopr Pitan(5): 48-51. Abstract: The authors studied the influence of linseed oil, and mixtures of linseed and sunflower oils, in varying ratios, on the levels of cholesterol, low- and very low-density lipoproteins, high-density cholesterol, free and esterified cholesterol, and on the fatty-acid composition of low- and very low-density lipoproteins. In experiments on Wistar white rats linseed oil decreased cholesterol concentration, and the levels of low- and very low-density lipoproteins, as well as affected the fatty-acid composition of lipoproteins. |
| Effect of lipid composition on lipoprotein lipase activity measured by a continuous fluorescence assay: effect of cholesterol supports an interfacial surface penetration model Lobo, L. I. and D. C. Wilton (1997), Biochem J 321 (Pt 3): 829-35. Abstract: The breakdown of normal substrates by lipases requires an interfacial binding step prior to hydrolysis. Interfacial binding and subsequent hydrolysis will be affected by the lipid components and hence physical properties of the substrate surface. In order to investigate in detail the effect of lipid structure on the activity of lipoprotein lipase (LPL), triolein-containing emulsion particles of defined composition have been used as substrates. In addition, lipase activity has been measured using a continuous fluorescence displacement assay that monitors the release of long-chain fatty acids as an alternative to normal radiochemical assays. Using this fluorescence assay, rates of hydrolysis of triolein were the same as when using a standard radiochemical assay under identical conditions. Activation by apolipoprotein CII was very similar by both methods; however, the extent of activation (2-3-fold) was less than has been reported previously using different assay conditions. In order to investigate the effect of cholesterol on LPL activity, emulsion particles were prepared in which the cholesterol/egg-phosphatidylcholine ratio was increased up to a 1:1 molar ratio. A pronounced stimulatory effect of cholesterol was observed under these assay conditions, with up to a 5-fold increase in rate compared with emulsion particles without cholesterol. Since high molar ratios of cholesterol are reported to exclude triacylglycerol from the phospholipid surface Spooner and Small (1987) Biochemistry 26, 5820-5825, these results are not consistent with a mechanism involving LPL hydrolysis of surface triacylglycerol. Instead, they support an interfacial penetration model, allowing the enzyme's active site direct access to triacylglycerol in the lipoprotein core. Perturbation of the surface phospholipid monolayer of the emulsion particle as a result of hydrolysis by Naja naja phospholipase A2 resulted in a 10-fold activation of LPL, providing further support for an interfacial penetration model. The stimulatory effect of apolipoprotein CII was not modulated by modification of the interface with cholesterol. |
| Effect of lipid content of diet on cholesterol content and cholesterogenic enzymes of European eel liver Burgos, C., M. F. Zafra, et al. (1993), Lipids 28(10): 913-6. Abstract: The effect of dietary lipid levels on the levels of cholesterol and the activities of the major cholesterogenic enzymes of the liver has been studied in the European eel. An increase in hepatic total cholesterol was observed when the dietary lipid levels increased from 12 to 20%, while protein levels were maintained at 30%. This change paralleled an increase in mevalonate 5-pyrophosphate decarboxylase activity, while 3-hydroxy-3-methylglutaryl-CoA reductase mevalonate kinase and mevalonate 5-phosphate kinase were not affected by changes in diet composition. These results suggest that the decarboxylase may be a rate-limiting enzyme in cholesterogenesis in eel liver. |
| Effect of lipidic factors on membrane cholesterol topology--mode of binding of theta-toxin to cholesterol in liposomes Ohno-Iwashita, Y., M. Iwamoto, et al. (1992), Biochim Biophys Acta 1109(1): 81-90. Abstract: We have previously suggested the existence of two distinct states for cholesterol in cell membranes as revealed by high- and low-affinity binding sites for theta-toxin of Clostridium perfringens. In liposomes, phospholipid and cholesterol compositions, but not membrane protein composition, have been shown to be major determinants for the topology of membrane cholesterol. The effects of lipidic factors on cholesterol topology were investigated in detail by analyzing toxin binding to large unilamellar liposomes composed of cholesterol and phospholipids (neutral phospholipids/phosphatidylglycerol = 82:18, mol/mol). The numbers of high- and low-affinity toxin-binding sites depend strictly on the cholesterol mole percentage in liposomes. High-affinity toxin-binding sites appear only in liposomes with high cholesterol contents. Liposomes whose cholesterol/phospholipid ratio is 0.4 or less have no high-affinity sites regardless of their phospholipid compositions, while low-affinity sites appear in liposomes with lower cholesterol contents. The threshold values for the cholesterol mole percentage above which high-affinity toxin-binding sites appear were examined. The values decrease in accordance with the increase in the mole fraction of 18-carbon hydrocarbon chains among the total 14-18 carbon-hydrocarbon chains of the liposomal phospholipids. Furthermore, both the partial replacement of phosphatidylcholine with phosphatidylethanolamine and the digestion of phospholipids with phospholipase C also affect the threshold values. Thus the cholesterol mole percentage, in combination with phospholipid chain length and other factors, determines the topology of membrane cholesterol providing distinctively different affinity sites for theta-toxin. |
| Effect of lipoproteins on cholesterol synthesis in rat Sertoli cells Maboundou, J. C., M. Fofana, et al. (1995), Biochem Cell Biol 73(1-2): 67-72. Abstract: Lipoprotein metabolism has been investigated in cultured rat Sertoli cells. Cells incubated with low-density lipoproteins (LDLs) or high-density lipoproteins (HDLs) showed a concentration-dependent decrease of sterol synthesis, indicating a net cholesterol delivery to the Sertoli cells. At 50 micrograms/mL, lipoproteins inhibited the incorporation of 14Cacetate into free cholesterol by 83% for the LDL and 47% for the HDL. Electron microscopic examinations of the Sertoli cells provide evidence of the internalization of gold-labelled HDL into coated pits and coated vesicles. Competitive studies between human LDL and rat HDL indicate that Sertoli cells take up cholesterol from LDL and HDL containing apolipoprotein (apo) E by common pathways. These results suggest that Sertoli cells possess apo B and E receptors for the uptake and degradation of LDL and HDL, although the basement membrane excludes the passage of LDL from blood capillaries to the Sertoli cells. At 50 micrograms/mL, apo-E-depleted HDL inhibited the incorporation of 14Cacetate into free cholesterol by 34%. Thus, this study shows that Sertoli cells are capable of taking up apo-E-depleted HDL cholesterol for cell metabolism. |
| Effect of liposome-encapsulated hemoglobin on triglyceride, total cholesterol, low-density lipoprotein, and high-density lipoprotein cholesterol measurements Abdullah, F., M. Whiteford, et al. (1997), Lipids 32(4): 377-81. Abstract: The present study investigated the effect of liposome-encapsulated hemoglobin (LEH), an experimental oxygen-carrying resuscitation fluid, on triglyceride, total cholesterol, and low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol measurements. In vivo, the intravenous infusion of LEH (5.6 mL/kg, n = 6) elevated serum triglycerides (+92% vs. baseline, P <.05), total cholesterol (+25% vs. baseline, P <.01), LDL cholesterol (+72% vs. baseline, P <.01) and had no effect on serum HDL cholesterol. In addition, LEH did not alter the elevation in serum triglycerides (+302% vs. baseline, P <.01) and LDL cholesterol (+86% vs. baseline, P <.01) induced by lipopolysaccharide (3.6 mg/kg, i.v., n = 6. Ex vivo, measurements of triglycerides and total cholesterol as well as LDL and HDL cholesterol in whole blood from naive rats were not changed by the addition of LEH (0-50%, n = 6). In vitro, the addition of a fixed concentration of LEH (50%, n = 6) to varying concentrations of cholesterol solution (0-50%), or vice versa, had no effect on cholesterol determination. It is therefore concluded that LEH only minimally affects serum levels of triglycerides, total cholesterol, LDL cholesterol, and HDL cholesterol and does not interfere with their measurement. |
| Effect of long-chain fatty acids on low-density-lipoprotein-cholesterol metabolism Woollett, L. A. and J. M. Dietschy (1994), Am J Clin Nutr 60(6 Suppl): 991S-996S. Abstract: The concentration of cholesterol in the low-density-lipoprotein (LDL) fraction of plasma is one of the major risk factors for coronary heart disease. Steady-state concentrations of LDL cholesterol in the plasma are determined primarily by the production rate and the rate of removal of LDL cholesterol from the circulation by receptor-dependent transport. The magnitude of these two processes is affected by the type of fatty acid in the diet. Saturated fatty acids with 14 and 16 carbon atoms suppress receptor-dependent LDL-cholesterol transport into the liver, increase the LDL-cholesterol production rate, and raise the plasma LDL-cholesterol concentration. The 9-cis 18:1 fatty acid restores receptor activity, lowers the production rate, and decreases the plasma LDL-cholesterol concentration. In contrast with these fatty acids, the 18:0 and 9-trans 18:1 fatty acids are biologically inactive and so do not change the circulating LDL-cholesterol concentration. |
| Effect of long-term beta-carotene and vitamin A on serum cholesterol and triglyceride levels among participants in the Carotene and Retinol Efficacy Trial (CARET) Redlich, C. A., J. S. Chung, et al. (1999), Atherosclerosis 145(2): 425-32. Abstract: OBJECTIVE: The Carotene and Retinol Efficacy Lung Cancer Chemoprevention Trial (CARET) ended prematurely due to the unexpected findings that the active treatment group on the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate had a 46% increased lung cancer mortality and a 26% increased cardiovascular mortality compared with placebo. This study was designed when the CARET intervention was halted to evaluate the effects of long-term supplementation with beta-carotene and retinol on serum triglyceride and cholesterol levels, in an attempt to explore possible explanations for the CARET result. METHODS: Serum triglyceride levels, and total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol levels were determined in a subgroup of 52 CARET participants. Baseline and mid-trial levels were available on 23 participants on placebo and 29 on active treatment who were then serially followed for 10 months after trial termination. RESULTS: Triglyceride, and total, HDL and LDL cholesterol levels were similar in the two groups at baseline. After a mean of 5 years on the intervention there was a small nonsignificant increase in serum triglyceride levels in the active group, but no difference in total, HDL, or LDL cholesterol levels. After stopping the intervention there was a decrease in triglyceride levels in the active intervention group, and no change in the other parameters. CONCLUSION: Based on a small convenience sample, CARET participants in the active treatment arm had a small nonsignificant increase in serum triglyceride levels while on the intervention, and a decrease in serum triglyceride levels after the intervention was discontinued. No significant changes in total or HDL cholesterol were noted. These results argue against a major contribution of treatment-induced changes in serum lipid and lipoprotein levels to the increased cardiovascular mortality in the active treatment group. |
| Effect of long-term hemodialysis on plasma lecithin: cholesterol acyltransferase activity and the amounts and compositions of HDL2 and HDL3 in hemodialysis-treated patients with chronic renal failure: a 9-year longitudinal study Mekki, K., M. Bouchenak, et al. (2004), Med Sci Monit 10(8): CR439-46. Abstract: BACKGROUND: Atherosclerosis was correlated with hemodialysis duration (HD) in chronic renal failure (CRF) patients. Dyslipidemias were identified as atherogenic risk factors. MATERIAL/METHODS: To investigate variations in HDL2 and HDL3 composition and lecithin: cholesterol acyltransferase (LCAT) activity as functions of HD, 20 CRF patients were selected for maintenance hemodialysis during the 9 years from April 1, 1991 to March 31, 2000. Blood samples were drawn four times: 1991 (T0, study begin), 1994 (T1), 1997 (T2), and 2000 (T3). T0 results were taken as references. RESULTS: Triacylglycerol concentrations were 1.12-fold higher at T1 (P<0.01), 1.31-fold at T2, and 1.63-fold at T3 (P<0.001). Increases of 14% and 33% of total cholesterol were noted at T2 (P<0.05) and T3 (P<0.001). Hypertriglyceridemia correlated with HD (r=0.70, P<0.05). LCAT activity decreased by 27%, 39%, and 51% at times T1, T2, and T3, respectively, this activity being negligible in 30% of patients at T2 and 40% at T3. An inverse relationship was noted between LCAT activity and HD (r=-0.80, P<0.001). Increases in HDL2-unesterified cholesterol (UC) and HDL3-UC were obtained at T2 and T3 (P<0.05), and high HDL2-triacylglycerols (TG) and HDL3-TG were noted at T1, T2, and T3 (P<0.001). HDL3-phospholipids (PL) values were diminished by 9% at T1 (P<0.05), 17% at T2, and 19% at T3 (P<0.001). CONCLUSIONS: Long-term hemodialysis aggravates lipid anomalies following CRF. Alterations in HDL composition contribute to the reduced efficacy of reverse cholesterol transport and patients are submitted to a greater risk for atherosclerosis. |
| Effect of lovastatin administered every other day on serum low-density lipoprotein cholesterol > 160 mg/dl Rindone, J. P., R. Achacoso, et al. (1995), Am J Cardiol 76(4): 312-3. Abstract: We undertook a pilot study examining the efficacy of lovastatin 20 mg every other day in patients with hypercholesterolemia, and found lovastatin to be effective in lowering low-density lipoprotein (LDL) levels in patients with serum LDL > 160 mg/dl. |
| Effect of lovastatin on acyl-CoA: cholesterol O-acyltransferase (ACAT) activity and the basolateral-membrane secretion of newly synthesized lipids by CaCo-2 cells Kam, N. T., E. Albright, et al. (1990), Biochem J 272(2): 427-33. Abstract: Lovastatin, a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity, was used to study the regulation of cholesterol metabolism and the basolateral-membrane secretion of triacylglycerol and cholesterol in the human intestinal cell line CaCo-2. At 0.1 microgram/ml, lovastatin decreased 3H2O incorporation into cholesterol by 71%. In membranes prepared from cells incubated with lovastatin for 18 h, HMG-CoA reductase activity was induced 4-8-fold. Mevalonolactone prevented this induction. In intact cells, lovastatin (10 micrograms/ml) decreased cholesterol esterification by 50%. The reductase inhibitor decreased membrane acyl-CoA:cholesterol O-acyltransferase (ACAT) activity by 50% at 5 micrograms/ml. ACAT inhibition by lavastatin was not reversed by adding excess of cholesterol or fatty acyl-CoA to the assay. Lovastatin, in the presence or absence of mevalonolactone, decreased the basolateral secretion of newly synthesized cholesteryl esters and triacylglycerols. Lovastatin also inhibited the esterification of absorbed cholesterol and the secretion of this newly synthesized cholesteryl ester. Lovastatin is a potent inhibitor of cholesterol synthesis in CaCo-2 cells. Moreover, it is a direct inhibitor of ACAT activity, independently of its effect on HMG-CoA reductase and cholesterol synthesis. |
| Effect of lovastatin on cholesterol absorption in cholesterol-fed rabbits Nielsen, L. B., S. Stender, et al. (1993), Pharmacol Toxicol 72(3): 148-51. Abstract: The aim of the present study was to investigate the effect of the hydroxymethylglutaryl (HMG)-CoA reductase inhibitor lovastatin on some aspects of cholesterol metabolism in cholesterol-fed rabbits. The plasma cholesterol concentration was markedly lower in lovastatin-treated rabbits (6 mg/rabbit/day) compared to controls after 36 days of cholesterol-feeding (x +/- S.E.) (19 +/- 4 mmol/l, n = 9 versus 153 +/- 17 mmol/l, n = 7) (P < 0.00001). Intestinal absorption of cholesterol in such rabbits was reduced by 15% in lovastatin-treated rabbits (n = 21) compared to controls (n = 18) (P < 0.025). The results suggest that the hypocholesterolaemic effect of lovastatin in cholesterol-fed rabbits is associated with a decreased intestinal absorption of cholesterol. |
| Effect of lovastatin on cholesterol content of cardiac and red blood cell membranes in normal and cardiomyopathic hamsters Pogue, D. H., C. S. Moravec, et al. (1995), J Pharmacol Exp Ther 273(2): 863-9. Abstract: Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, is used therapeutically to lower plasma cholesterol levels. However, the effect of this therapy on cell membrane cholesterol in vivo is not known. The goal of this study was to investigate whether lovastatin treatment of hamsters decreases cholesterol in cardiac cell membranes and in red blood cell (RBC) membranes. Because abnormal cellular Ca++ regulation has been associated with altered membrane cholesterol in hearts of cardiomyopathic (CM) hamsters, we also measured the cholesterol content of cardiac and RBC membranes from lovastatin-treated and untreated Bio 14.6 CM hamsters to determine whether any differences existed with respect to normals. Sarcolemma-enriched cardiac membranes and RBC membranes were obtained from 42 to 45-day normal and CM hamsters after 13 days of lovastatin treatment (0.1% of food/day) and from untreated normal and CM hamsters. Plasma cholesterol, membrane cholesterol/phospholipid (C/PL) ratio and cholesterol per milligram of membrane protein (C/prot) were determined. In hearts from untreated CM hamsters, C/prot was significantly lower (P <.05) than in untreated normals. Lovastatin decreased plasma cholesterol by 76% and 81% in normal and CM hamsters, respectively (P <.001), but after lovastatin treatment, there was no significant change in C/PL or C/prot in cardiac membranes from either strain; there was also no significant decrease in C/prot or in C/PL of RBC membranes from normals or C/PL of CM hamster RBC membranes. However, lovastatin feeding resulted in a significant (P <.01) 24% decrease in C/prot of CM RBC membranes.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effect of low dose atorvastatin versus diet-induced cholesterol lowering on atherosclerotic lesion progression and inflammation in apolipoprotein E*3-Leiden transgenic mice Verschuren, L., R. Kleemann, et al. (2005), Arterioscler Thromb Vasc Biol 25(1): 161-7. Abstract: OBJECTIVE: To evaluate whether low-dose atorvastatin suppresses atherosclerotic lesion progression and inflammation in apolipoprotein E*3 (apoE*3)-Leiden mice beyond its cholesterol-lowering effect. METHODS AND RESULTS: ApoE*3-Leiden mice were fed a high-cholesterol (HC) diet until mild atherosclerotic lesions had formed. Subsequently, HC diet feeding was continued or mice received HC supplemented with 0.002% (w/w) atorvastatin (HC+A), resulting in 19% plasma cholesterol lowering, or mice received a low-cholesterol (LC) diet to establish a plasma cholesterol level similar to that achieved in the HC+A group. HC+A and LC diet reduced, significantly and to the same extent, lesion progression and complication in the aortic root, as assessed by measuring total atherosclerotic lesion area, lesion severity, and macrophage and smooth muscle cell area. In the aortic arch, HC+A but not LC blocked lesion progression. HC+A and LC reduced vascular inflammation (ie, expression of macrophage migration inhibitory factor, plasminogen activator inhibitor- 1, matrix metalloproteinase-9), but HC+A additionally suppressed vascular cell adhesion molecule-1 expression and, in parallel, monocyte adhesion. In contrast, low-dose atorvastatin showed no antiinflammatory action toward hepatic inflammation markers (serum amyloid A, C-reactive protein CRP) in apoE*3-Leiden mice and human CRP transgenic mice. CONCLUSIONS: Low-dose atorvastatin cholesterol-dependently reduces lesion progression in the aortic root but shows antiinflammatory vascular activity and tends to retard atherogenesis in the aortic arch beyond its cholesterol-lowering effect. |
| Effect of low-density lipoprotein buoyant density and cholesterol content on the formation of lipoprotein(a) particles Becker, L., B. R. Gabel, et al. (2001), Clin Exp Med 1(2): 121-5. Abstract: Lipoprotein(a) Lp(a) is a unique lipoprotein which resembles low-density lipoprotein (LDL) both in lipid composition and the presence of apolipoprotein B-100 (apo B-100). Lp(a) is, however, distinguishable from LDL by the presence of an additional glycoprotein apolipoprotein(a) apo(a), which is covalently attached to apo B-100 by a single disulfide bond. It is now generally accepted that Lp(a) assembly is a two-step process in which the initial non-covalent interaction between apo(a) and apo B-100 is mediated by the weak lysine binding sites present in kringle IV types 6, 7 and 8 of apo(a). In the present study, we have investigated the effect of LDL heterogeneity on Lp(a) assembly in a group of 111 individuals. The three parameters of LDL composition assessed in this study were the cholesterol content, the apo B content, and the relative flotation rate (a measure of LDL buoyancy and thus size). We found no correlation between the size of LDL particles and the extent of Lp(a) formation; a weak negative correlation was observed between cholesterol content of LDL and Lp(a) formation (P=0.042). This may suggest a role for free (i.e., surface-associated) cholesterol in the ability of LDL to form Lp(a) particles. |
| Effect of low-density lipoprotein cholesterol apheresis on blood viscosity Moriarty, P. M., C. A. Gibson, et al. (2004), Am J Cardiol 93(8): 1044-6. Abstract: Few studies have been designed to study the hemodynamic effects of low-density lipoprotein apheresis, especially on whole blood viscosity. Six patients with cardiovascular disease and hypercholesterolemia underwent a single low-density lipoprotein apheresis, resulting in significant reductions in whole blood viscosity at all shear rates. |
| Effect of low-dose simvastatin on cholesterol levels, oxidative susceptibility, and antioxidant levels of low-density lipoproteins in patients with hypercholesterolemia: a pilot study Yoshida, H., T. Ishikawa, et al. (1995), Clin Ther 17(3): 379-89. Abstract: In this pilot study, 12 patients (6 men, 6 postmenopausal women) with hypercholesterolemia were treated with low-dose (5 mg/d) simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, for 4 weeks. Low-density lipoprotein (LDL) samples were isolated at the beginning (week 0) and at the end (week 4) of the treatment regimen. Simvastatin caused significant decreases of total cholesterol (-18.1%), LDL cholesterol (-27.6%), and apolipoprotein B (-21.8%), and significantly reduced total cholesterol, free cholesterol, cholesterol esters, phospholipids, and protein in LDL without significantly changing the component ratios and fatty acid levels of LDL. However, simvastatin therapy had no major effects on either antioxidant levels in LDL or the oxidative susceptibility of LDL. We conclude that low-dose simvastatin significantly reduces LDL cholesterol levels without increasing the oxidative susceptibility of LDL or decreasing the antioxidant levels of LDL, and thus may reduce the risk of coronary artery disease. |