| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol vaccines Bailey, J. M. (1994), Science 264(5162): 1067-8. |
| Cholesterol values and the fasting state Fraser, G. E. (1990), Jama 264(23): 3063, 3067. |
| Cholesterol values in a cohort of adolescents in Sor Trondelag Resellmo, K. and E. W. Nielsen (1998), Tidsskr Nor Laegeforen 118(12): 1852-3. Abstract: Over a four-year period total serum cholesterol values were obtained from all 7th grade lower secondary school students (age 13) in a municipality in Norway. The 139 girls included in the survey had a mean value of 4.24 mmol/l (95% CI 4.12-4.37), and the 160 boys 4.11 mmol/l (95% CI 3.98-4.23), which is slightly lower than other Nordic surveys. Some students from one year were also measured in the 9th and 11th grades. One student was found to have familial hyper-cholesterolemia, and this value was excluded from the reference material. Screening for this disease among students is not recommended. |
| Cholesterol values of an elderly person Viikari, J. (2002), Duodecim 118(3): 217-9. |
| Cholesterol vehicle in experimental atherosclerosis 24: avocado oil Kritchevsky, D., S. A. Tepper, et al. (2003), J Am Coll Nutr 22(1): 52-5. Abstract: OBJECTIVE: To determine atherogenicity of avocado oil relative to saturated (coconut oil), monounsaturated (olive oil) and polyunsaturated (corn oil) fats. METHODS: New Zealand White rabbits were fed a semipurified diet containing 0.2% cholesterol and 14% fat for 90 days. They were then necropsied and severity of atherosclerosis was determined visually. RESULTS: Coconut oil was the most atherogenic fat. Corn oil was only slightly less atherogenic than either olive or avocado oils. Percentage of serum HDL cholesterol was highest in the rabbits fed the two monounsaturated fats. CONCLUSION: Avocado oil is of the same order of atherogenicity as corn oil and olive oil. |
| Cholesterol vehicle in experimental atherosclerosis. 23. Effects of specific synthetic triglycerides Kritchevsky, D., S. A. Tepper, et al. (2000), Lipids 35(6): 621-5. Abstract: Earlier work has shown that increasing concentration of palmitic acid at the sn-2 position of a fat enhances the atherogenic properties of that fat. This effect has been observed with lard, tallow, cottonseed oil, and palm oil. In the experiment reported here, we have studied the atherogenic effects of four synthetic fats fed to rabbits as 58% (w/w) of the total fat (15%) (w/w) of a semipurified diet containing 0.05% cholesterol. The fats being tested were: 1,3-stearoyl-2-oleoylglycerol (SOS); 1,2-stearoyl-3-oleoylglycerol (SSO); 1,3-palmitoyl-2-oleoylglycerol (POP); and 1,2-palmitoyl-3-oleoylglycerol (PPO). After 20 wk on diet there were no differences among the groups in weight gain, liver weight, serum, or liver lipids. These data are consistent with our previous findings. There were significant differences in atherosclerosis. The most severe atherosclerosis was observed in group PPO and the least in groups SSO and POP. Severity of atherosclerosis was graded visually on a 0-4 scale. The average atherosclerosis (aortic arch and thoracic aorta) divided by 2 was: SOS--1.35; SSO--0.97; POP--0.83; and PPO--1.80. Fecal fat excretion (an indicator of fat absorption) was higher in the two groups fed the stearic acid-rich fats and lower in groups fed the palmitic acid-rich fats. There were no differences in low density lipoprotein particle size. The results confirm previous findings concerning the increased atherogenicity of fats bearing palmitic acid at the sn-2 position. The mechanism underlying these observations is moot but may, in part, reflect greater absorption of the atherogenic fat. |
| Cholesterol versus alpha-tocopherol: effects on properties of bilayers made from heteroacid phosphatidylcholines Stillwell, W., T. Dallman, et al. (1996), Biochemistry 35(41): 13353-62. Abstract: The techniques of differential scanning calorimetry, fluorescence of merocyanine 540, fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene, proton permeability, and lipid peroxidation are used to compare the perturbations of cholesterol and alpha-tocopherol on lipid bilayer membranes composed of different phosphatidylcholines containing stearic acid in the sn-1 position and an unsaturated fatty acid (either oleic, alpha-linolenic, gamma-linolenic, or docosahexaenoic acid) in the sn-2 position. It is concluded that the structural roles of cholesterol and alpha-tocopherol may be similar with membranes composed of some phosphatidylcholines but are clearly different with membranes composed of other related phosphatidylcholines. alpha-Tocopherol exerts a much larger effect than cholesterol on membranes rich in polyunsaturated fatty acids that have their initial double bond before the delta 9 position. Cholesterol interacts more favorably with fatty acids that do not have an double bond before the delta 9 position. The membrane structural effects are explained in terms of the larger size of the sterol ring structure of cholesterol compared to the smaller chromanol ring of the alpha-tocopherol. |
| Cholesterol versus cholesterol sulfate: effects on properties of phospholipid bilayers containing docosahexaenoic acid Schofield, M., L. J. Jenski, et al. (1998), Chem Phys Lipids 95(1): 23-36. Abstract: The important omega-3 fatty acid docosahexaenoic acid (DHA) is present at high concentration in some membranes that also contain the unusual sterol cholesterol sulfate (CS). The association between these lipids and their effect on membrane structure is presented here. Differential scanning calorimetry (DSC), MC540 fluorescence, erythritol permeability, pressure/area isotherms on lipid monolayers and molecular modeling are used to compare the effect of CS and cholesterol on model phospholipid membranes. By DSC, CS decreases the main phase transition temperature and broadens the transitions of dipalmitolyphosphatidylcholine (DPPC), 1-stearoyl-2-oleoyl-sn-glycero-3-phosphocholine (18:0,18:1 PC) and 1-stearoyl-2-docosahexaenoyl-sn-glycero-3-phosphocholine (18:0,22:6 PC) to a much larger extent than does cholesterol. In addition CS produces a three-component transition in 18:0,18:1 PC bilayers that is not seen with cholesterol. In a mixed phospholipid bilayer composed of 18:0,18:1 PC/18:0,22:6 PC (1:1, mol/mol), CS at 2.5 membrane mol% or more induces lateral phase separation while cholesterol does not. CS decreases lipid packing density and increases permeability of 18:0,18:1 PC and 18:0,22:6 PC bilayers to a much larger extent than cholesterol. CS disrupts oleic acid-containing bilayers more than those containing DHA. Molecular modeling confirms that the anionic sulfate moiety on CS renders this sterol more polar than cholesterol with the consequence that CS likely resides higher (extends further into the aqueous environment) in the bilayer. CS can therefore be preferentially accommodated into DHA-enriched bilayers where its tetracyclic ring system may fit into the delta 4 pocket of DHA, a location excluded to cholesterol. It is proposed that CS may in part replace the membrane function of cholesterol in DHA-rich membranes. |
| Cholesterol vesicles in areas of gastric metaplasia of gallbladder epithelium Caselli, M., A. Aleotti, et al. (1996), J Submicrosc Cytol Pathol 28(2): 251-3. Abstract: Gastric metaplasia is a frequent epithelial change in gallbladder of lithiasic patients. Particles consistent with cholesterol-containing vesicles were searched in areas overlying gastric metaplastic cells, in gastric metaplastic cells, in areas overlying normal-looking epithelial cells and in normal-looking epithelial cells in 25 patients with radiolucent calculi and 10 control patients undergoing cholecystectomy for other reasons. Important trends were found confirming the peculiar role of mucous layer adherent to metaplastic gallbladder epithelium in beginning the nucleation process and interesting pictures concerning the formation of uni- and multilamellar vesicles in these "nucleating areas" were seen. |
| Cholesterol(free cholesterol, esterified cholesterol) Maeba, R. and H. Shimasaki (2001), Nippon Rinsho 59 Suppl 2: 14-20. |
| Cholesterol, A beta and Alzheimer's disease Hartmann, T. (2001), Trends Neurosci 24(11 Suppl): S45-8. Abstract: Statins have been used for many years for the treatment of hypercholesterolemia. They lower low-density lipoprotein (LDL) cholesterol, increase high-density lipoprotein (HDL) levels and are considered to be very safe. Recently, a set of potential new applications was identified for statins. In the future, these drugs could be used to treat Alzheimer's disease (AD). Past studies have suggested a link between AD and lipids and a series of reports has recently been published that significantly tightens this link and also provides some explanations at the cellular level. This review focuses on these recent developments and perspectives that appear to link cholesterol, beta-amyloid and AD. |
| Cholesterol, a cell size-dependent signal that regulates glucose metabolism and gene expression in adipocytes Le Lay, S., S. Krief, et al. (2001), J Biol Chem 276(20): 16904-10. Abstract: Enlarged fat cells exhibit modified metabolic capacities, which could be involved in the metabolic complications of obesity at the whole body level. We show here that sterol regulatory element-binding protein 2 (SREBP-2) and its target genes are induced in the adipose tissue of several models of rodent obesity, suggesting cholesterol imbalance in enlarged adipocytes. Within a particular fat pad, larger adipocytes have reduced membrane cholesterol concentrations compared with smaller fat cells, demonstrating that altered cholesterol distribution is characteristic of adipocyte hypertrophy per se. We show that treatment with methyl-beta-cyclodextrin, which mimics the membrane cholesterol reduction of hypertrophied adipocytes, induces insulin resistance. We also produced cholesterol depletion by mevastatin treatment, which activates SREBP-2 and its target genes. The analysis of 40 adipocyte genes showed that the response to cholesterol depletion implicated genes involved in cholesterol traffic (caveolin 2, scavenger receptor BI, and ATP binding cassette 1 genes) but also adipocyte-derived secretion products (tumor necrosis factor alpha, angiotensinogen, and interleukin-6) and proteins involved in energy metabolism (fatty acid synthase, GLUT 4, and UCP3). These data demonstrate that altering cholesterol balance profoundly modifies adipocyte metabolism in a way resembling that seen in hypertrophied fat cells from obese rodents or humans. This is the first evidence that intracellular cholesterol might serve as a link between fat cell size and adipocyte metabolic activity. |
| Cholesterol, a modulator of membrane-associated Abeta-fibrillogenesis McLaurin, J., A. A. Darabie, et al. (2003), Pharmacopsychiatry 36 Suppl 2: S130-5. Abstract: One of the major pathological features of Alzheimer's disease is the presence of extracellular amyloid plaques that are predominantly composed of the amyloid-beta peptide (Abeta). Characterisation of plaques demonstrated the predominance of two peptides differing at the carboxyl terminus by 2 hydrophobic amino acids, Abeta40 and Abeta42. Diffuse plaques associated with AD are composed predominantly of Abeta42, whereas senile plaques contain both Abeta40 and Abeta42. Recently, it has been suggested that diffuse plaque formation is initiated as a plasma membrane bound Abeta species and that Abeta42 is the critical component. In order to investigate this hypothesis, we have examined Abeta40/42-lipid interactions using in situ atomic force microscopy, electron microscopy and fluorescence anisotropy. While the association of Abeta42 with planar bilayers resulted in peptide aggregation but no fibre formation, this was not the case for Abeta40 where we observed preferential fibre formation. Cholesterol, a key membrane component and modulating factor in AD, is inversely correlated with the extent of Abeta40/42-bilayer interaction. These results were confirmed using fluorescence anisotropy to evaluate the effect of Abeta on membrane fluidity and fluorimetry to confirm membrane integrity. Our results suggest that the enhanced amyloidogenic properties of Abeta42 are not correlated with fibril formation but aggregation on bilayer surfaces. |
| Cholesterol, a modulator of membrane-associated Abeta-fibrillogenesis and neurotoxicity Yip, C. M., E. A. Elton, et al. (2001), J Mol Biol 311(4): 723-34. Abstract: Recent studies have suggested that cholesterol, an important determinant of the physical state of biological membranes, plays a significant role in the development of Alzheimer's disease. We have employed in situ scanning probe microscopy, fluorescence anisotropy, and electron microscopy to investigate how cholesterol levels within total brain lipid bilayers effect amyloid beta-peptide (Abeta)-assembly. Fluorescence anisotropy measurements revealed that the relative fluidity of the total brain lipid membranes was influenced by the level of cholesterol and the addition of Abeta40 resulted in a decrease in the overall vesicle fluidity. In situ scanning probe microscopy performed on supported planar bilayers of total brain lipid revealed a correlation between membrane fluidity, as influenced by cholesterol level, and the extent of Abeta-insertion and subsequent fibrillogenesis. These observations were consistent with fluorescence microscopy studies of PC-12 and SH-SY5Y cell lines exposed to exogenous Abeta, which revealed an inverse correlation between membrane cholesterol level, and Abeta-cell surface binding and subsequent cell death. These results collectively suggest that Abeta-cell surface interactions are mediated by cellular cholesterol levels, the distribution of cholesterol throughout the cell, and membrane fluidity. |
| Cholesterol, apolipoproteins, and the risk of myocardial infarction Crook, D., I. F. Godsland, et al. (1992), N Engl J Med 326(7): 490-1; discussion 491-2. |
| Cholesterol, apolipoproteins, and the risk of myocardial infarction Myers, R. I. (1992), N Engl J Med 326(7): 491; author reply 491-2. |
| Cholesterol, apolipoproteins, and the risk of myocardial infarction Rosenson, R. S. (1992), N Engl J Med 326(7): 491; author reply 491-2. |
| Cholesterol, apolipoproteins, and the risk of myocardial infarction Simon, J. A., W. S. Browner, et al. (1992), N Engl J Med 326(7): 491; author reply 491-2. |
| Cholesterol, atherosclerosis and cerebro-cardiovascular complications in 3,236 elderly autopsy cases Kuramoto, K., S. Ueda, et al. (1991), Nippon Ronen Igakkai Zasshi 28(2): 188-93. Abstract: The effect of serum cholesterol on aortic, cerebral, coronary and femoral atherosclerosis as well as on the incidence of cerebral and myocardial infarctions were analyzed in 3,236 consecutive autopsies in the elderly. Serum cholesterol levels declined over the age of 80 in both genders. The cholesterol levels of females were significantly higher than that of males in each age group from the sixties through the nineties. The increase in serum cholesterol was correlated with the progression of coronary atherosclerosis in both genders, but not with cerebral or femoral atherosclerosis. Slight progression of aortic atherosclerosis was observed when serum cholesterol was over 160 mg/dl. Cholesterol induced progression of coronary atherosclerosis was found in cases with hypertension, but not in the normotensive group. In accordance with the progression of coronary atherosclerosis, the incidence of myocardial infarction increased with an elevation of serum cholesterol levels, and this relationship between myocardial infarction and cholesterol levels was found only in patients with hypertension. No correlation was found between the incidence of cerebral infarction and serum cholesterol levels. It was concluded that hypercholesterolemia in the elderly is a risk factor of myocardial infarction in cases with hypertension, but is not a risk factor of cerebral infarction. |
| Cholesterol, beta-sitosterol, ergosterol, and coprostanol in agricultural soils Puglisi, E., M. Nicelli, et al. (2003), J Environ Qual 32(2): 466-71. Abstract: In this work we analyzed the sterol content of agricultural soils. Three eukaryotic sterols, cholesterol, beta-sitosterol, and ergosterol were chosen as representative of the animal, plant, and fungal kingdoms, while coprostanol was validated as a marker of human fecal matter contamination. Three soils subjected to different treatments (sewage sludge application, irrigation by saline waters, and contamination by industrial and municipal wastes) were sampled and their sterol content was measured and compared with adjacent untreated soils. The effects of time, location, and treatment were evaluated by means of a number of statistical techniques. Beta-sitosterol concentration varied from 0.9 to 30 mg kg(-1). Lesser values were measured in Cremona (2.1 mg kg(-1)) than in Bari (4.0 mg kg(-1)) and Naples (10.9 mg kg(-1)) soils. No significant effects were detected for cholesterol and ergosterol. Coprostanol was present after sewage sludge disposal and contamination by industrial and municipal wastes, while it was absent in the soil treated with saline water and in the adjacent untreated soil. Coprostanol concentration did not vary much within site and time of sampling, with a mean value of 0.2 mg kg(-1). We confirmed coprostanol as a useful persistent marker of human fecal matter contamination. Multivariate analysis highlighted a clear distinction between the eukaryotic sterols and coprostanol. In addition, a different behavior between ergosterol and cholesterol on one side and beta-sitosterol on the other was detected. This preliminary work suggests that sterols deserve a deeper study of their use as indicators in agricultural soils. |