| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Cholesterol-multilipid interactions in bilayers Finegold, L. and M. A. Singer (1991), Chem Phys Lipids 58(1-2): 169-73. Abstract: To extend our knowledge of model membrane systems based upon one lipid component, multi-lamellar bilayers were made of cholesterol with two phospholipids in equimolar ratio, and the enthalpy change delta H of the main phase transition of the temary mixture was measured by differential scanning calorimetry (DSC) as a function of increasing cholesterol concentration c. The lipids were saturated phosphatidylcholines CnPC of acyl chain length n, and as the n of the two lipids became more different (from C13PC/C14PC to C14PC/C15PC to C14PC/C18PC to C14PC/C19PC) distinct breaks in the delta H versus c plots were observed. These mixtures displayed only one broad DSC endotherm. Mixtures of an unsaturated lipid C18: 1PC (dioleoyl) with C16PC or with C18PC showed two peaks, with each peak being associated with its parent lipid. However, the delta H versus c plots for each of these peaks showed an initial independence of cholesterol concentration followed by a dependence on cholesterol concentration. These results indicate that, in lipid mixtures, the type of interaction of cholesterol with each lipid component depends on the concentration of cholesterol present. |
| Cholesterol--now what? Smith, P. (2001), Tidsskr Nor Laegeforen 121(9): 1022. |
| Cholesterol--once again la Cour Petersen, E. (1990), Ugeskr Laeger 152(8): 545-6. |
| Cholesterolosis is not associated with high cholesterol levels in patients with and without gallstone disease Mendez-Sanchez, N., M. A. Tanimoto, et al. (1997), J Clin Gastroenterol 25(3): 518-21. Abstract: High levels of cholesterol have been associated with certain gallbladder disorders such as cholesterolosis and gallstone disease. Furthermore, obesity is considered the main risk factor for cholesterol gallstone disease. We investigated the incidence of cholesterolosis in patients with and patients without gallbladder stones (GS). We reviewed the clinical records of patients with gallstone disease and other gallbladder disorders who had consecutive cholecystectomy during a 5-year period. We recorded demographic data, sex, age, serum cholesterol levels, and body mass index. The diagnosis of cholesterolosis was made macroscopically and microscopically. A total of 636 patients were included in this study: 446 with and 190 without GS. Cholesterolosis was more frequent in patients without GS (p < 0.01). However, hypercholesterolemia occurred more frequently in patients with GS (p < 0.001). Obese patients with GS had higher percentages of cholesterolosis and hypercholesterolemia than did eutrophic patients (p < 0.01 and p < 0.05, respectively). We suggest that cholesterolosis in the human gallbladder is not necessarily associated with gallstone disease and high plasma cholesterol levels. |
| Cholesterolosis. Incidence, correlation with serum cholesterol level and the role of laparoscopic cholecystectomy Khairy, G. A., S. Y. Guraya, et al. (2004), Saudi Med J 25(9): 1226-8. Abstract: OBJECTIVE: To report the incidence of cholesterolosis in the surgically removed gallbladders, its association with serum cholesterol level and to review the role of laparoscopic cholecystectomy in the treatment. METHODS: This retrospective study included all patients who had consecutive cholecystectomies for various gallbladder disorders, performed by 2 consultants during a 5-year period from January 1997 through to December 2002, in the College of Medicine and King Khalid University Hospital, King Saud University, Riyadh, Kingdom of Saudi Arabia. The clinical records of those found to have cholesterolosis on histopathological examination were reviewed, and the data were analyzed for their age, sex, fasting serum cholesterol level and the final outcome of cholecystectomy. RESULTS: The study group was comprised of 549 patients and out of which, 74 (13.4%) had cholesterolosis of the gallbladder. There were 59 (79.9%) female and 15 (20.1%) male patients. Age ranged from 18-64-years with a mean of 35.7-years. Sixty-three (85.1%) cases were reported to have abnormally high fasting serum cholesterol levels (>=5.5 mmol/L), whereas 11 (14.9%) had normal serum cholesterol level. Cholesterolosis with coexistent gallstones was documented in 47 (63.3%) patients while 27 (36.5%) subjects showed acalculous cholesterolosis. Laparoscopic cholecystectomy was performed in 71 (95.9%) individuals, whereas 3 patients ended up with open cholecystectomy (conversion rate of 4.2%). There were no postoperative complications. CONCLUSION: Cholesterolosis of the gallbladder is a distinct pathologic entity and carries a positive correlation with high serum cholesterol level. Laparoscopic cholecystectomy is effective, safe and a feasible treatment modality for cholesterolosis. |
| Cholesterol-producing transgenic Caenorhabditis elegans lives longer due to newly acquired enhanced stress resistance Lee, E. Y., Y. H. Shim, et al. (2005), Biochem Biophys Res Commun 328(4): 929-36. Abstract: Because Caenorhabditis elegans lacks several components of the de novo sterol biosynthetic pathway, it requires sterol as an essential nutrient. Supplemented cholesterol undergoes extensive enzymatic modification in C. elegans to form other sterols of unknown function. 7-Dehydrocholesterol reductase (DHCR) catalyzes the reduction of the Delta7 double bond of sterols and is suspected to be defective in C. elegans, in which the major endogenous sterol is 7-dehydrocholesterol (7DHC). We microinjected a human DHCR expression vector into C. elegans, which was then incorporated into chromosome by gamma-radiation. This transgenic C. elegans was named cholegans, i.e., cholesterol-producing C. elegans, because it was able to convert 7DHC into cholesterol. We investigated the effects of changes in sterol composition on longevity and stress resistance by examining brood size, mean life span, UV resistance, and thermotolerance. Cholegans contained 80% more cholesterol than the wild-type control. The brood size of cholegans was reduced by 40% compared to the wild-type control, although the growth rate was not significantly changed. The mean life span of cholegans was increased up to 131% in sterol-deficient medium as compared to wild-type. The biochemical basis for life span extension of cholegans appears to partly result from its acquired resistance against both UV irradiation and thermal stress. |
| Cholesterol-raising effects of coffee: clues to regulation of cholesterol metabolism Grundy, S. M. (1995), J Intern Med 238(6): 475-7. |
| Cholesterol-raising factor from boiled coffee does not pass a paper filter van Dusseldorp, M., M. B. Katan, et al. (1991), Arterioscler Thromb 11(3): 586-93. Abstract: Previous studies have indicated that consumption of boiled coffee raises total and low density lipoprotein (LDL) cholesterol, whereas drip-filtered coffee does not. We have tested the effect on serum lipids of consumed coffee that was first boiled and then filtered through commercial paper coffee filters. Sixty-four healthy volunteers consumed six cups per day of this boiled and filtered coffee for 17 days. Then, they were randomly divided into three groups, which, for the next 79 days, received either unfiltered boiled coffee (lipid content, 1.0 g/l), boiled and filtered coffee (0.02 g lipid/l), or no coffee. Serum total cholesterol levels rose by 0.42 mmol/l (16 mg/dl; 95% confidence interval CI, 0.14-0.71), LDL cholesterol levels by 0.41 mmol/l (16 mg/dl; 95% CI, 0.16-0.66), and apolipoprotein B levels by 8.6 mg/dl (95% CI, 3.8-13.4) in those who consumed boiled coffee relative to those who consumed boiled and filtered coffee. Responses of triglycerides, high density lipoprotein cholesterol, and apolipoprotein A-I did not differ significantly among these groups. No significant effects on serum lipid levels were found in the boiled and filtered coffee-consuming group compared with those who drank no coffee. In subjects who drank boiled coffee, serum campesterol level, an indicator of cholesterol absorption, remained constant. The serum lathosterol level, an indicator of cholesterol synthesis, increased by 11% (p less than 0.05), but the lathosterol to cholesterol ratio did not change. We propose that paper filters of the type used for drip-filtered coffee retain the lipid present in boiled coffee and in that way remove the hypercholesterolemic factor.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol-receptor-mediated genomics in health and disease Kaul, D. (2003), Trends Mol Med 9(10): 442-9. Abstract: Cross-talk between cell-surface receptor C(k) and intracellular receptors (liver X receptor-alpha and peroxisome-proliferator-activated receptors) controls a set of crucial genes that maintain a finely orchestrated balance between various cellular processes involved in cell growth, differentiation, apoptosis, cholesterol homeostasis and inflammation. Abnormal cross-talk of these receptors can lead to several human diseases, particularly atherosclerosis, cancer and autoimmune diseases. As our understanding of the complex signaling events that link these receptors to human health improves, we are beginning to appreciate the enormous potential of the proposed cross-talk model of cholesterol receptors in the prevention and/or treatment of diseases. |
| Cholesterol-reducing medications-a new therapeutic option for multiple sclerosis? Statins as immunomodulators Neuhaus, O., H. Wiendl, et al. (2003), Nervenarzt 74(8): 704-7. Abstract: Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is crucial for cholesterol biosynthesis, and are widely used as lipid-lowering agents. These drugs greatly reduce atherosclerosis and cardiovascular morbidity, which in the past was mainly attributed to their cholesterol-lowering properties. However, recent evidence suggests that statins are also potent immunomodulators. They exerted beneficial effects on animal models of experimental autoimmune encephalomyelitis and thus have therapeutic potential for multiple sclerosis. Their exact mechanism of action is still unclear. HMG-CoA-dependent effects and a direct effect on immune receptors are conceivable and are reviewed here. |
| Cholesterol-reducing therapy of arteriosclerosis Mabudhi, H. (1998), Nippon Naika Gakkai Zasshi 87(3): 540-7. |
| Cholesterol-related knowledge, attitudes, and behaviors in a low-income, urban patient population Hyman, D. J., D. G. Simons-Morton, et al. (1993), Am J Prev Med 9(5): 282-9. Abstract: To determine knowledge, attitudes, behaviors, and self-reported cholesterol measurement in a low-income, urban patient population, we conducted an interview survey of users and potential users of primary care services in a public health care system for low-income Harris County, Texas, residents. The response rate was 93%, with a final sample of 547 randomly selected subjects 18 years of age and older, who were Hispanic (54%), black (28%), non-Hispanic white (14%), and Asian, Native American, or other (4%). Results indicated that 76% had heard of serum or blood cholesterol, and 30% reported past cholesterol measurement. Knowledge that dietary saturated fat can raise blood cholesterol ranged from 11% in Hispanic men to 51% in non-Hispanic white men and women. A lower percentage of Hispanics correctly answered all knowledge questions, and Hispanics reported higher-fat food choices than blacks and non-Hispanic whites. More than 90% of the respondents expressed interest in more information on diet, 60% reported that they read nutrition labels, and 15% said they have been trying to reduce blood cholesterol levels. A lower percentage of Hispanics reported previous cholesterol measurement than blacks or non-Hispanic whites, a difference that persisted after adjusting for multiple factors associated with cholesterol measurement. Older age (older than 50) and more physician visits in the past year also were associated with past cholesterol measurement. Comparisons with national surveys show that cholesterol knowledge and actual measurement in this low-income sample lag behind those of the national population. Yet, despite gaps in knowledge and cholesterol measurement, respondents showed positive attitudes about and interest in cholesterol-lowering interventions. |
| Cholesterol-rich diet induced changes in plasma lipids in relation to apolipoprotein E phenotype in healthy students Lehtimaki, T., T. Moilanen, et al. (1992), Ann Med 24(1): 61-6. Abstract: The hypothesis that apolipoprotein E (apoE) polymorphism modulates an individual's response to cholesterol-rich diet was tested in 36 healthy normolipidaemic students with apoE phenotypes E3/2 (n = 9), E3/3 (n = 11), E4/3 (n = 13) and E4/4 (n = 3). The subjects were instructed to eat their usual diets, omitting eggs, for three weeks (baseline). This was followed by a diet high in cholesterol (750 mg/day, from egg yolks) for three weeks (intervention) after which they returned to their normal diet (without eggs for three weeks). Concentrations of plasma lipids and apolipoprotein B, and the composition of total fatty acids were monitored. At baseline, there were no statistically significant differences in lipid concentrations between the phenotype groups. The cholesterol-rich diet induced significant increases in total cholesterol, LDL cholesterol, and apoB in all apoE groups (P less than 0.001). The magnitudes of these increases were similar in groups E3/2, E3/3, and E4/3, in which total cholesterol concentration rose by 13%, 18%, and 12%, respectively. Stronger responses were observed in the small group of E4/4 subjects, in whom the increases in total cholesterol, LDL cholesterol, and apoB were 2.3-fold (P = 0.054), 2.25-fold (P = 0.02) and 2.3-fold (P = 0.004), respectively, compared with all the other phenotypes studied. |
| Cholesterol-rich LDL perfused at physiological LDL-cholesterol concentration induces platelet aggregation and PAF-acetylhydrolase activation Chui, D. H., F. Marotta, et al. (1991), Biomed Pharmacother 45(1): 37-42. Abstract: The aim of this research was to perform an in vivo study on the relationships between lipid oxide (LP), platelet aggregation and PAF-acetylhydrolase in a model using perfusion of cholesterol-rich LDL media diluted to physiological LDL-cholesterol concentration. Normal rabbits were infused with LDL (d 1.025-1.063 g/ml) extracted from rabbits previously fed either with standard food (I-LDL group), 1% cholesterol food (II-LDL group) or 1% cholesterol plus probucol (IV-LDL group). CU2+ modified II-LDL was also infused (III-LDL group). After dilution as above, LP increased significantly in III- and II-LDL media. After perfusion, LP significantly increased in III- and II-LDL groups as compared to baseline values and to control. Compared to the I-LDL group, PAF-acetylhydrolase and platelet aggregation significantly increased in III- and II-LDL groups. These data indicate the property of cholesterol- rich LDL to activate PAF-acetylhydrolase and enhance platelet aggregation, even when perfused through a medium containing a physiological LDL-cholesterol concentration. |
| Cholesterol-rich lipid rafts mediate akt-regulated survival in prostate cancer cells Zhuang, L., J. Lin, et al. (2002), Cancer Res 62(8): 2227-31. Abstract: Although cholesterol accumulation in tumors was first reported in the early20th century, the mechanistic implications of this observation are still obscure. Here we report that caveolin-negative human prostate cancer (LNCaP) cells contain cholesterol-rich lipid rafts that mediate epidermal growth factor (EGF)-induced and constitutive signaling through the Akt1 serine-threonine kinase. EGF receptor and Akt1 phosphorylation were inhibited and autonomous cell survival was reduced when the rafts were disrupted. Reconstitution of the rafts with cholesterol restored EGF receptor-->Akt1 axis signaling and cytoprotection from a phosphoinositide 3-kinase-dependent apoptotic signal. These results suggest that cholesterol present in membrane microdomains is a prominent mediator of survival in prostate cancer cells. |
| Cholesterol-rich plasma membrane domains (lipid rafts) in keratinocytes: importance in the baseline and UVA-induced generation of reactive oxygen species Gniadecki, R., N. Christoffersen, et al. (2002), J Invest Dermatol 118(4): 582-8. Abstract: The biologic effects of ultraviolet radiation such as DNA damage, mutagenesis, cellular aging, and carcinogenesis are in part mediated by reactive oxygen species. In unirradiated cells the major known sources of reactive oxygen species are the mitochondrial respiratory chain and the membrane oxidases functionally coupled to several membrane growth factor receptors. There is evidence that mitochondria also play a role in oxidative stress after ultraviolet irradiation; however, it is unknown whether the biochemical processes at the level of the plasma membrane contribute to the regulation of reactive oxygen species synthesis. In order to elucidate this issue we examined here the importance of the microdomain plasma membrane organization in the regulation of oxidative stress in unirradiated and ultraviolet A (340-400 nm) irradiated HaCaT keratinocytes. Labeling of confluent HaCaT cultures with fluorescently tagged cholera toxin B subunit (FITC-CTx) revealed the presence of GM1 ganglioside and cholesterol-rich microdomains (lipid rafts) that formed junction-like structures in the membranes of adjacent cells and patchy microdomains elsewhere. There was a marked heterogeneity in the level of FITC-CTx labeling: there were groups of cells demonstrating prominent labeling (FITC-CTx(high)) whereas other cells were only weakly labeled (FITC-CTx(low)). When reactive oxygen species synthesis was measured with the fluorescent probe carboxy-2',7'-dichlorodihydrofluorescein diacetate, we found that (i) the baseline and ultraviolet-A-induced reactive oxygen species synthesis correlated with the magnitude of FITC-CTx labeling and was highest in the FITC-CTx(high) cells; (ii) reactive oxygen species synthesis was diminished in cells in which the integrity of membrane domains was disrupted by cholesterol sequestration with methyl-beta-cyclodextrin and filipin, or after treatment with GM1 ganglioside; (iii) reactive oxygen species synthesis in cholesterol-depleted cells was fully restored after cholesterol repletion. We conclude that the plasma membrane takes part in the regulation of oxidative stress in keratinocytes and disruption of its microdomain structure reduces reactive oxygen species synthesis both at the baseline and after ultraviolet A irradiation. We hypothesize that lipid-raft-associated protein(s) may be involved in the generation of reactive oxygen species and that pharmacologic modulation of membrane structure may provide a novel therapeutic approach relevant for photoprotection and cutaneous carcinogenesis. |
| Cholesterol-rich rabbit serum modulates beta-adrenergic receptor density of human lymphocytes. A possible role of LDL-cholesterol Pieri, C., F. Moroni, et al. (1992), Ann N Y Acad Sci 650: 239-44. Abstract: The effect of in vitro treatment of human lymphocytes with rabbit cholesterol-rich serum (RCS) on the membrane microviscosity as well as on the beta-adrenergic receptor density has been investigated. RCS treatment of cells resulted in a 30% decrease of receptor density without any effect on membrane microviscosity. A complete recovery was observed incubating the RCS cells either with the "Active Lipids" (AL) or with heparin. The AL are a mixture of neutral lipids, phosphatidylcholine and phosphatidylethanolamine from hen egg yolk known to fluidify the cell membrane. The AL modified membrane microviscosity of control lymphocytes without altering their beta-receptor number. These observations support the proposition that beta-receptor density of human lymphocytes is not regulated by membrane microviscosity and suggest that probably low density lipoprotein-cholesterol complex is involved in such a regulation. |
| Cholesterol-rich thyroglossal cyst: report of a case diagnosed by fine needle aspiration Chow, L. T., J. C. Lee, et al. (1996), Acta Cytol 40(2): 377-9. |
| Cholesterol-sensor initiates M. tuberculosis entry into human macrophages Kaul, D., P. K. Anand, et al. (2004), Mol Cell Biochem 258(1-2): 219-22. Abstract: Cholesterol-mediated mycobacteria entry into and survival within macrophages has added a new dimension to Tuberculosis research. The molecular mechanism through which cholesterol initiates this process is still poorly understood. The present study addressed to resolve this mechanism revealed that Mycobacterium tuberculosis possesses cholesterol-specific Receptor 'Ck'-like molecule responsible for mycobacterial entry into macrophages. Further human Receptor-Ck was found to regulate transcriptional expression of a gene that codes for Tryptophan-Aspartate containing coat (TACO) protein responsible for survival of mycobacteria within cells. Based upon these results, we propose that interaction of Receptor-Ck with cholesterol-rich membrane domains helps to create a 'Synaptic-junction' between mycobacteria and macrophage resulting in signalling events that are responsible for mycobacterium entry into and survival within macrophages. |
| Cholesterol-specific probe for lipoproteins immobilized on nitrocellulose membranes Smejkal, G. B. and H. F. Hoff (1994), Biotechniques 16(1): 68-70. |