| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| The effect of cholesterol and dicetylphosphate on the physical parameters of liposomes Bondar, O. P., P. A. Voziian, et al. (1994), Biofizika 39(2): 323-7. Abstract: The physical parameters of liposomes from phosphatidylcholine with cholesterol or dicetylphosphate were investigated. The sizes, electrophoretic mobility, surface density charges of these liposomes were estimated. It has been shown that dicetylphosphate, as well as cholesterol increases the thickness of bilayer of the lecithin liposomes and at the same time the area occupied by one lipid molecule has not been changed by dicetylphosphate in contrast to cholesterol. |
| The effect of cholesterol and epicholesterol on the activity and temperature dependence of the purified, phospholipid-reconstituted (Na+ + Mg2+)-ATPase from Acholeplasma laidlawii B membranes George, R. and R. N. McElhaney (1992), Biochim Biophys Acta 1107(1): 111-8. Abstract: The (Na+ + Mg2+)-ATPase purified from Acholeplasma laidlawii B membranes was reconstituted into large, unilamellar vesicles formed from dimyristoylphosphatidylcholine (DMPC) and varying amounts of cholesterol or epicholesterol. The ATP hydrolytic activity of the reconstituted enzyme was then determined over a range of temperatures and the phase state of the DMPC in the ATPase-containing vesicles was characterized by high-sensitivity differential scanning calorimetry. In the vesicles containing only DMPC, the ATPase activity is higher in association with lipids in the liquid-crystalline state than with gel-state phospholipids, resulting in a curvilinear, biphasic Arrhenius plot with a pronounced change in slope at the elevated gel to liquid-crystalline phase transition temperature of the DMPC. The incorporation of increasing amounts of cholesterol into the DMPC vesicles results in a progressively greater degree of inhibition of ATPase activity at higher temperatures but a stimulation of activity at lower temperatures, thus producing Arrhenius plots with progressively less curvature and without an abrupt change in slope at physiological temperatures. As cholesterol concentration in the ATPase-DMPC vesicles increases, the calorimetric phase transition of the phospholipid is further broadened and eventually abolished. The incorporation of epicholesterol into the DMPC proteoliposomes results in similar but less pronounced effects on ATPase activity, and its effect on the phase behavior of the DMPC-ATPase vesicles is also similarly attenuated in comparison with cholesterol. Moreover, cholesterol added to the purified enzyme in the absence of phospholipid does not show any significant effect on either the activity or the temperature dependence of the detergent-solubilized ATPase. These findings are consistent with the suggestion that cholesterol exerts its effect on the ATPase activity by altering the physical state of the phospholipid, since the ordering effect of cholesterol (or epicholesterol) on liquid-crystalline lipid results in a reduction of ATPase activity while the disordering of gel-state lipid results in an increase in activity. |
| The effect of cholesterol and monosialoganglioside (GM1) on the release and aggregation of amyloid beta-peptide from liposomes prepared from brain membrane-like lipids Tashima, Y., R. Oe, et al. (2004), J Biol Chem 279(17): 17587-95. Abstract: In order to investigate the influence of cholesterol (Ch) and monosialoganglioside (GM1) on the release and subsequent deposition/aggregation of amyloid beta peptide (Abeta)-(1-40) and Abeta-(1-42), we have examined Abeta peptide model membrane interactions by circular dichroism, turbidity measurements, and transmission electron microscopy (TEM). Model liposomes containing Abeta peptide and a lipid mixture composition similar to that found in the cerebral cortex membranes (CCM-lipid) have been prepared. In all, four Abeta-containing liposomes were investigated: CCM-lipid; liposomes with no GM1 (GM1-free lipid); those with no cholesterol (Ch-free lipid); liposomes with neither cholesterol nor GM1 (Ch-GM1-free lipid). In CCM liposomes, Abeta was rapidly released from membranes to form a well defined fibril structure. However, for the GM1-free lipid, Abeta was first released to yield a fibril structure about the membrane surface, then the membrane became disrupted resulting in the formation of small vesicles. In Ch-free lipid, a fibril structure with a phospholipid membrane-like shadow formed, but this differed from the well defined fibril structure seen for CCM-lipid. In Ch-GM1-free lipid, no fibril structure formed, possibly because of membrane solubilization by Abeta. The absence of fibril structure was noted at physiological extracellular pH (7.4) and also at liposomal/endosomal pH (5.5). Our results suggest a possible role for both Ch and GM1 in the membrane release of Abeta from brain lipid bilayers. |
| The effect of cholesterol in a liposomal Muc1 vaccine Batenjany, M. M., L. T. Boni, et al. (2001), Biochim Biophys Acta 1514(2): 280-90. Abstract: A liposomal Muc1 mucin vaccine for treatment of adenocarcinomas was formulated by incorporating a synthetic Muc1 mucin-based lipopeptide and Lipid A into a DPPC/cholesterol bilayer. Vaccination of mice with the liposomal formulation produced a peptide-specific immune response dependent on the cholesterol content. The response occurred at a threshold of 20-23 mol% cholesterol, and was optimal at cholesterol levels of > or =30 mol%. To understand this cholesterol dependency, we studied the effect of cholesterol on the liposomal bilayer and surface properties. Freeze-fracture electron microscopy showed a unique surface texture that was codependent upon cholesterol (> or =20 mol%) and lipopeptide content. Fluorescence anisotropy measurements exhibited a significant decrease in the rotational motion of 1,6-diphenyl-1,3,5-hexatriene in formulations containing >20 mol% cholesterol and only in the presence of the lipopeptide. At 20 mol% cholesterol and with lipopeptide, DSC showed a significant increase in the main phase transition of the DPPC bilayers, while Raman spectroscopy indicated a more ordered arrangement of DPPC molecules compared to control liposomes containing DPPC/cholesterol alone. Taken together, the data suggest the presence of lipopeptide-rich microdomains at and above a threshold of 20 mol% cholesterol that may play a role in the induction of a peptide-specific immunological response. |
| The effect of cholesterol level in erythrocyte membranes on the sedimentation rate, electrophoretic motility, and the rate of potassium ferricyanide reduction Balmukhanov, B. S., K. E. Bulegenov, et al. (1990), Biofizika 35(2): 293-6. Abstract: It has been found that with an increase of the molar ratio cholesterol/phospholipids in human erythrocyte membranes in vitro their sedimentation rate in diluted suspensions increases and the reduction rate of potassium ferricyanide decreases, while the electrophoretic mobility of erythrocytes is not changed. The effect of cholesterols discussed in terms of the mechanism of transmembrane transfer of reduction equivalents and non-equilibrium in the double electric layer of erythrocytes surface. |
| The effect of cholesterol level in liposomes on the interaction with blood serum lipoproteins Zakharova, T. S., A. S. Ivanov, et al. (1994), Biokhimiia 59(5): 712-9. Abstract: The effect of the cholesterol content in liposomes on their interaction with blood serum lipoproteins has been studied. It was shown that phosphatidyl choline liposomes without cholesterol did not interact selectively with any class of serum lipoproteins. At the same time, addition of high cholesterol concentrations to liposomes confers to them a new feature, namely the ability to interact selectively with the serum low density lipoproteins. Up to 90% of such lipoproteins can interact with liposomes. This finding was confirmed by "in vivo" data. The observed effect of "address" properties given to liposomes by a native lipid may be of interest in search for new possibilities to use liposomes for selective delivery of drugs. |
| The effect of cholesterol lowering on carotid and femoral artery wall stiffness and thickness in patients with familial hypercholesterolaemia Smilde, T. J., F. W. van den Berkmortel, et al. (2000), Eur J Clin Invest 30(6): 473-80. Abstract: BACKGROUND: Early in the process of atherosclerosis, changes in vessel wall stiffness and thickness may occur. The present study evaluates the effect of cholesterol reduction on artery wall stiffness and intima media thickness in patients with familial hypercholesterolaemia (FH). MATERIALS AND METHODS: Forty-five patients with familial hypercholesterolaemia (mean age 46+/-10 years) with untreated LDL cholesterol concentration > 9 mmol L(-1), were studied before and after one year of cholesterol lowering therapy with statins (simvastatin, atorvastatin 40-80 mg day(-1). The distensibility (DC in 10-3 kPa(-1) and compliance (CC in mm2. kPa(-1) of the common carotid artery (CCA) (right and left side) and common femoral artery (CFA) (right side) were determined by a wall track system (Pie Medical). The intima media thickness (IMT) (both right and left) of the CCA, bulb (BUL), internal carotid artery (ICA) and CFA were measured in mm by high-resolution ultrasound (Biosound). RESULTS: The mean concentration of total cholesterol (TC), LDL-cholesterol (LDL-C) and triglycerides (TG) were reduced significantly by 43%, 51% and 25%, respectively, whereas HDL-cholesterol (HDL-C) increased by 13% (P<0.001). In the CFA, the DC and CC increased significantly (DC from 7.9+/-3.0 to 9.1+/-3.7 in 10(-3) kPa(-1); CC 0.5+/-0.2-0.6+/-0.3 in mm2. kPa(-1), whereas the DC and CC did not change in the CCA. In contrast, the IMT of the CCA decreased significantly in both men and women whereas an IMT decrease was also seen in the BUL and ICA in premenopausal women. A LDL-cholesterol reduction of 44.8% and 45.4% was necessary to induce significant decreases in IMT and increases in DC and CC. CONCLUSIONS: One year of cholesterol lowering therapy in FH decreases the wall stiffness in the CFA and the arterial wall thickness in the CCA. |
| The effect of cholesterol on membrane potentials, proliferation and migration of cultivated endothelial cells Mende, S., I. Windeck, et al. (1992), Pharmazie 47(12): 930-3. Abstract: The influence of cholesterol added as cholesterol containing liposomes sphingomyelin/cholesterol (1: 1; mol/mol) or as cholesterol suspensions on cultured bovine aortic endothelial cells was investigated. 10(-6) mol/l cholesterol enhanced membrane potential, 10(-5) mol/l caused depolarisation. The proliferation of the cells was dependent on the concentration influenced in opposite directions too. The proliferation was stimulated by 10(-6) mol/l cholesterol and inhibited by 10(-5) mol/l. The migratory rate of the cells was increased by 10(-6) mol/l and 10(-5) mol/l cholesterol. Our results suggest that exogenous cholesterol is integrated in membranes of the endothelial cells and causes in this way changes of membrane potential, proliferation rate and migratory activity. |
| The effect of cholesterol on parameters of gramicidin D ion channels and on the macroscopic and microscopic characteristics of lipid bilayers Hianik, T., G. Laputkova, et al. (1991), Cesk Fysiol 40(2): 113-32. |
| The effect of cholesterol on the accumulation of intracellular calcium Zhou, Q., S. Jimi, et al. (1991), Biochim Biophys Acta 1085(1): 1-6. Abstract: Cholesterol/egg phosphatidylcholine (PC) liposomes (1:1 or 4:1, M/M), in which the absolute amount of PC was adjusted to be the same, were incubated with cultured bovine arterial smooth muscle cells for up to 8 h at 37 degrees C. The effect of increased cellular cholesterol on the accumulation of intracellular calcium in these cells was studied. The results indicate that the intracellular calcium content, measured by Fura-2/AM, was increased 2.3-fold by incubation with 4:1, cholesterol/PC liposomes. Kinetic analysis using 45Ca2+ indicated that the increased calcium influx was due to increase of pool size, not from a change of rate constant. (Ca2+ + Mg2+)-ATPase activity was decreased by 4:1, cholesterol/PC liposomes. The molar ratio of cholesterol/phospholipids in the cell membranes was directly proportional to that in liposomes. No change in phospholipid composition was noted. We suggest that the accumulation of intracellular calcium was a composite result due to the altering effect of inserted cholesterol on surface area, and to direct interactions between cholesterol and the proteins of the Ca2+ channel and (Ca2+ + Mg2+)-ATPase. |
| The effect of cholesterol on the lateral diffusion of phospholipids in oriented bilayers Filippov, A., G. Oradd, et al. (2003), Biophys J 84(5): 3079-86. Abstract: Pulsed field gradient NMR was utilized to directly determine the lipid lateral diffusion coefficient for the following macroscopically aligned bilayers: dimyristoylphosphatidylcholine (DMPC), sphingomyelin (SM), palmitoyloleoylphosphatidylcholine (POPC), and dioleoylphosphatidylcholine (DOPC) with addition of cholesterol (CHOL) up to approximately 40 mol %. The observed effect of cholesterol on the lipid lateral diffusion is interpreted in terms of the different diffusion coefficients obtained in the liquid ordered (l(o)) and the liquid disordered (l(d)) phases occurring in the phase diagrams. Generally, the lipid lateral diffusion coefficient decreases linearly with increasing CHOL concentration in the l(d) phase for the PC-systems, while it is almost independent of CHOL for the SM-system. In this region the temperature dependence of the diffusion was always of the Arrhenius type with apparent activation energies (E(A)) in the range of 28-40 kJ/mol. The l(o) phase was characterized by smaller diffusion coefficients and weak or no dependence on the CHOL content. The E(A) for this phase was significantly larger (55-65 kJ/mol) than for the l(d) phase. The diffusion coefficients in the two-phase regions were compatible with a fast exchange between the l(d) and l(o) regions in the bilayer on the timescale of the NMR experiment (100 ms). Thus, strong evidence has been obtained that fluid domains (with size of micro m or less) with high molecular ordering are formed within a single lipid bilayer. These domains may play an important role for proteins involved in membrane functioning frequently discussed in the recent literature. The phase diagrams obtained from the analysis of the diffusion data are in qualitative agreement with earlier published ones for the SM/CHOL and DMPC/CHOL systems. For the DOPC/CHOL and the POPC/CHOL systems no two-phase behavior were observed, and the obtained E(A):s indicate that these systems are in the l(d) phase at all CHOL contents for temperatures above 25 degrees C. |
| The effect of cholesterol on the morphology and reactivity of the mixture of lipids used in syphilis serology Orum, O., J. R. Nielsen, et al. (1990), Apmis 98(1): 9-18. Abstract: The effect of increasing amounts of cholesterol on the morphology of the liposomes constituting the VDRL-antigen was studied. The morphological parameters examined were the shape of the lipoidal particles and especially the number of lamellae on each particle in the various mixtures of lipids studied. Cholesterol in the presence of cardiolipin and lecithin is observed as rhomboid crystals, indicating that the majority of the cholesterol is located exterior to the lamellar membranes of lecithin and cardiolipin. It is shown that the effect of cholesterol is to reduce the number of individual lamellae per liposome, mainly by mechanically dispersing the cardiolipin and lecithin on the surface of the cholesterol crystals. It is suggested that cholesterol has no effect on the structure of the epitopes which react with antibodies in sera from patients with syphilis, but that, as a result of the mechanical dispersion of cardiolipin and lecithin, it creates liposomes with more accessible epitopes. |
| The effect of cholesterol oxidation products on human platelet aggregation Selley, M. L., J. A. McGuiness, et al. (1996), Thromb Res 83(6): 449-61. Abstract: The cholesterol oxidation products (oxysterols) cholest-3,5-diene-7-one, cholestan-5 alpha, 6 alpha-epoxy-3 beta-ol (cholesterol 5 alpha-epoxide), cholestan-5 beta, 6 beta-epoxy-3 beta-ol (cholesterol 5 beta-epoxide), cholest-5-ene-3 beta-ol-7-one (7-ketocholesterol), cholest-5-ene-3 beta, 7 alpha-diol (7 alpha-hydroxycholesterol), cholestan-3 beta, 5 alpha, 6 beta-triol (cholestane triol), and cholest-5-ene-3 beta, 26-diol (27-hydroxycholesterol) potentiated platelet aggregation and increased thromboxane A2 formation in platelets challenged with thrombin, ADP or collagen. These effects were observed at oxysterol concentrations in the range 5-100 microM. Cholesterol 5 beta-epoxide and 7-ketocholesterol increased the mobilization of 3H-arachidonic acid from prelabelled platelet phospholipids in response to thrombin and collagen. |
| The effect of cholesterol reduction on the endothelial function and progression of atherosclerosis in WHHL rabbits Kroon, A. A., A. F. Stalenhoef, et al. (1993), Atherosclerosis 103(2): 221-30. Abstract: In 3-month-old homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits the effect of treatment with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor pravastatin was studied for 9 months and related to the endothelial function of the coronary arteries of isolated hearts and rings of the distal abdominal aorta. Oral administration of pravastatin in doses up to 40 mg/kg per day significantly decreased plasma cholesterol by 51% in comparison to untreated WHHL rabbits. Basal coronary flow and bradykinin-induced increase in coronary flow in Langendorff hearts of the pravastatin-treated animals were significantly greater than the flow in the control animals, whereas the metacholine-induced relaxation of abdominal aortic rings was not different and attenuated in comparison to New Zealand white rabbits. The incidence of atherosclerotic lesions in four main coronary arteries and the aorta was significantly lower in the pravastatin treated animals (25.0% and 52.8% respectively) than in untreated WHHL rabbits (34.1% and 80.0% respectively). The mean percentage of narrowing in the aorta was also significantly lower in the pravastatin-treated group (12.0%) than in the controls (25.2%). Significant correlations were found between the extent of atherosclerotic lesions and the bradykinin-induced increase in coronary flow versus plasma total cholesterol levels. Thus, in this model, long term cholesterol lowering treatment with pravastatin starting at an early age retards the progression of plaque formation and preserves the endothelium-dependent relaxation of the coronary arteries. |
| The effect of cholesterol-lowering agents on hepatic and plasma cholesterol in Niemann-Pick disease type C Patterson, M. C., A. M. Di Bisceglie, et al. (1993), Neurology 43(1): 61-4. Abstract: Niemann-Pick disease type C (NP-C) is a neurovisceral lipidosis characterized by defective intracellular trafficking of cholesterol and lysosomal accumulation of unesterified cholesterol, believed to be an offending metabolite. We studied the effect of cholesterol-lowering agents on hepatic and plasma cholesterol levels in NP-C by randomly assigning 25 patients with NP-C to one of five treatment regimens containing different combinations of cholestyramine, lovastatin, nicotinic acid, or dimethyl sulfoxide (DMSO). Unesterified cholesterol content was measured in liver biopsies before and after 4 months' treatment. All drug regimens except DMSO alone reduced hepatic and plasma cholesterol levels. Toxicity was limited and did not prevent any patient from completing the study. The combination of cholestyramine, lovastatin, and nicotinic acid lowered cholesterol levels in liver and blood with minimal side effects. A controlled clinical study will be necessary to determine if this regimen influences the rate of neurologic progression. |
| The effect of cholesteryl ester transfer protein -629C->A promoter polymorphism on high-density lipoprotein cholesterol is dependent on serum triglycerides Borggreve, S. E., H. L. Hillege, et al. (2005), J Clin Endocrinol Metab 90(7): 4198-204. Abstract: CONTEXT: The -629C-->A cholesteryl ester transfer protein (CETP) promoter polymorphism is a determinant of HDL cholesterol (HDL-C). The effect of the closely linked CETP TaqIB polymorphism on HDL-C has been suggested to be modified by obesity and hyperinsulinemia. OBJECTIVE: Because the CETP-mediated cholesteryl ester transfer out of HDL is stimulated by high triglycerides, we hypothesized that triglycerides modify the effect of the CETP -629C-->A promoter polymorphism on HDL-C. DESIGN: In 7083 nondiabetic subjects of the PREVEND population, the -629C-->A promoter polymorphism, HDL-C, serum triglycerides, waist circumference, and insulin resistance (HOMA(ir)) were determined. Serum apolipoprotein A-I was available in 6948 subjects. The TaqIB polymorphism was also assessed. SETTING: The study is set in the general community. RESULTS: HDL-C and serum apolipoprotein A-I were on average 0.14 mmol/liter and 0.05 g/liter higher in -629AA (22.9%) compared to -629CC (26.8%) homozygotes (P < 0.001 for both). This genotype effect on HDL-C was on average 0.15 mmol/liter in the lowest triglyceride tertile but only 0.08 mmol/liter in the highest tertile (P < 0.01). Multiple regression analysis showed that HDL-C was determined by the CETP promoter variant (P < 0.001), gender (P < 0.001), triglycerides (P < 0.001), and interactions between triglycerides and genotype (P < 0.05), between triglycerides and gender (P < 0.05), and between genotype and gender (P < 0.05), independently from waist, HOMA(ir), alcohol use, age, and use of lipid-lowering drugs. The TaqIB polymorphism also interacted with triglycerides on HDL-C. The -629C-->A promoter polymorphism did not interact with obesity and HOMA(ir) on HDL-C. CONCLUSIONS: The HDL-C-raising effect of the CETP -629A allele is diminished with higher triglycerides, which may be explained by a predominant effect of triglyceride-rich lipoproteins over circulating CETP itself on cholesteryl ester transfer out of HDL with rising triglycerides. |
| The effect of chromium picolinate on serum cholesterol and apolipoprotein fractions in human subjects Press, R. I., J. Geller, et al. (1990), West J Med 152(1): 41-5. Abstract: Chromium has been implicated as a cofactor in the maintenance of normal lipid and carbohydrate metabolism. A deficiency of chromium results from diets low in biologically available chromium. Picolinic acid, a metabolite of tryptophan, forms stable complexes with transitional metal ions, which results in an improved bioavailability of the metal ion chromium. To determine whether or not chromium picolinate is effective in humans, 28 volunteer subjects were given either chromium tripicolinate (3.8 micromol 200 micrograms chromium) or a placebo daily for 42 days in a double-blind crossover study. A 14-day period off capsules was used between treatments. Levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoprotein B, the principal protein of the LDL fraction, decreased significantly while the subjects were ingesting chromium picolinate. The concentration of apolipoprotein A-I, the principal protein of the high-density lipoprotein (HDL) fraction, increased substantially during treatment with chromium picolinate. The HDL-cholesterol level was elevated slightly but not significantly during ingestion of chromium picolinate. Only apolipoprotein B, of the variables measured, was altered significantly during supplementation with the placebo. These observations show that chromium picolinate is efficacious in lowering blood lipids in humans. |
| The effect of coffee consumption on serum cholesterol levels Kokjohn, K., M. Graham, et al. (1993), J Manipulative Physiol Ther 16(5): 327-35. Abstract: OBJECTIVE: Studies investigating the association of coffee consumption and serum cholesterol levels report conflicting results. In an attempt to resolve this controversy, we reviewed the literature to answer the question: Is there a true positive association between coffee consumption and serum cholesterol levels? DATA SOURCES: A Medline database search dating back to 1965 was utilized. Key words used in the search were coffee, caffeine and cholesterol. Cholesterol was expanded to include lipoproteins and LDL-, HDL- and VLDL-cholesterol. All articles that presented cholesterol data in association with coffee consumption were examined for references missed by Medline. Recently published articles were located by a hand search through Current Contents and the latest monthly editions of Index Medicus. STUDY SELECTION: Three reviewers made the decision to include all publications that met the following criteria: a) reported original experimental results; b) reported total serum cholesterol levels; and c) were published in peer-reviewed journals. DATA EXTRACTION: Two to four articles were read and analyzed each week in chronological order. Independent data extraction was performed by three reviewers, who then met as a group once a week to cross-check the analyses. DATA SYNTHESIS: A trend, representing the association between coffee consumption and serum cholesterol, was calculated for each study. The trend was based on the percent difference in cholesterol values between subjects drinking four or more cups of coffee per day in comparison to those drinking zero or less than one cup of coffee each day. In order to compare studies that reported different cup sizes and different levels of intake, weighted mean cholesterol levels were calculated. In studies discussing the data in terms of correlations, trends were established according to the r values provided by the authors. CONCLUSIONS: The majority of studies demonstrated a positive trend in at least one subpopulation of their subjects, indicating that serum cholesterol levels increase with increasing coffee consumption. Stronger trends were seen among subjects drinking boiled coffee than in those drinking filtered, decaffeinated or instant coffee. However, most studies were not randomized clinical trials, and results can be countered by a number of biases prevalent in the studies, indicating the need for additional well-designed investigations to resolve remaining issues. |
| The effect of coffee on serum cholesterol level Grobbee, D. E. (1991), Ned Tijdschr Geneeskd 135(10): 438-9. |
| The effect of coffee on serum cholesterol level Meijler, F. L. (1991), Ned Tijdschr Geneeskd 135(9): 391. |