| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| The cholesterol controversy Geurian, K. L. (1996), Ann Pharmacother 30(5): 495-500. Abstract: OBJECTIVE: To provide information about the controversy associated with lowering of cholesterol concentrations to prevent coronary heart disease (CHD). DATA SOURCES: Studies, review articles, and editorials identified from MEDLINE searches (from 1966 to 1995) and bibliographies of identified articles. STUDY SELECTION: Studies, review articles, and editorials addressing controversial issues related to cholesterol lowering. DATA EXTRACTION: Pertinent information was selected and the data synthesized into a review format. DATA SYNTHESIS: Hypercholesterolemia is a well-known CHD risk factor. Reduction of serum cholesterol concentrations has been shown to reduce the incidence of CHD. Unfortunately, cholesterol lowering also appears to increase the risk for cancer, accidental and violent death, stroke, and oddly enough, CHD when certain medications are used. CONCLUSIONS: Significant reductions in serum cholesterol concentrations can be achieved with cholesterol-lowering interventions. However, the benefits associated with cholesterol reduction may not outweigh the risks in all patients with hypercholesterolemia. Cholesterol-lowering interventions should be recommended with caution in patients at increased risk of cancer, stroke, and depression. Caution should also be used when recommending fibric acid derivatives for patients with existing CHD. |
| The cholesterol controversy O'Connor, M. (1992), Bmj 304(6828): 711. |
| The cholesterol controversy Reckless, J. P. (1992), Bmj 304(6828): 712. |
| The cholesterol controversy Ryan, M. F., A. Moran, et al. (1992), Bmj 304(6828): 711-2. |
| The cholesterol controversy Schrott, H. and P. Palumbo (1990), Iowa Med 80(7): 349-51. |
| The cholesterol controversy Tobert, J. A. (1992), Bmj 304(6828): 713. |
| The cholesterol controversy Winder, T. (1992), Bmj 304(6828): 712-3. |
| The cholesterol controversy: is cholesterol really a risk factor for coronary artery disease? Margolis, S. (1991), Trans Assoc Life Insur Med Dir Am 74: 69-77. |
| The cholesterol debate Ballantyne, D. and M. Kelly (1992), Practitioner 236(1510): 87-90. |
| The cholesterol dependence of activation and fast desensitization of the nicotinic acetylcholine receptor Rankin, S. E., G. H. Addona, et al. (1997), Biophys J 73(5): 2446-55. Abstract: When nicotinic acetylcholine receptors are reconstituted into lipid bilayers lacking cholesterol, agonists no longer stimulate cation flux. The kinetics of this process are difficult to study because variations in vesicle morphology cause errors in flux measurements. We developed a new stopped-flow fluorescence assay to study activation independently of vesicle morphology. When receptors were rapidly mixed with agonist plus ethidium, the earliest fluorescence increase reported the fraction of channels that opened and their apparent rate of fast desensitization. These processes were absent when the receptor was reconstituted into dioleoylphosphatidylcholine or into a mixture of that lipid with dioleoylphosphatidic acid (12 mol%), even though a fluorescent agonist reported that resting-state receptors were still present. The agonist-induced channel opening probability increased with bilayer cholesterol, with a midpoint value of 9 +/- 1.7 mol% and a Hill coefficient of 1.9 +/- 0.69, reaching a plateau above 20-30 mol% cholesterol that was equal to the native value. On the other hand, the observed fast desensitization rate was comparable to that for native membranes from the lowest cholesterol concentration examined (5 mol%). Thus the ability to reach the open state after activation varies with the cholesterol concentration in the bilayer, whereas the rate of the open state to fast desensitized state transition is unaffected. The structural basis for this is unknown, but an interesting corollary is that the channels of newly synthesized receptors are not fully primed by cholesterol until they are inserted into the plasma membrane--a novel form of posttranslational processing. |
| The cholesterol derivative of a triantennary galactoside with high affinity for hepatic asialoglycoprotein receptor: a potent cholesterol lowering agent Biessen, E. A., H. Broxterman, et al. (1995), J Med Chem 38(11): 1846-52. Abstract: Cholesterol-derivatized galactosides have been devised in order to induce liver uptake of lipoproteins via the galactose-recognizing asialoglycoprotein receptor in the liver. In this study we describe the derivatization of a newly developed triantennary cluster galactoside having high affinity for the asialoglycoprotein receptor, N-tris-O-(3,6,9-trioxaundecanyl-beta-D-galactopyranosyl)metho xym ethyl -N alpha-1-(6-methyladipyl)glycinamide (TG(20A)) with cholesterol. Hereto, TG(20A) was coupled to glycine-(5-cholesten-3 beta-yl ester) in the presence of (benzotriazol-1-yloxy)tris(dimethylamino)phosphonium hexafluorophosphate, affording N-tris-O-(3,6,9-trioxaundecanyl-beta-D- galactopyranosyl)methoxymethylmethyl-N alpha-1-(6-(5-cholesten-3 beta-yloxy)glycyl)adipylglycinamide (TG(20A)C) in 46% yield. This compound is an amphiphilic, water-soluble compound. In aqueous solution it readily formed small micelles (4.9 +/- 1.2 nm) consisting of approximately 20 molecules. Upon incubation with human serum, TG(20A)C spontaneously incorporated into the most prominent serum lipoproteins, i.e., low-density lipoprotein (LDL) and high-density lipoprotein (HDL), thereby inducing an increase in buoyant density of these lipoproteins. The integrity of HDL and LDL, as judged from particle size analysis of both lipoproteins, was not altered by incubation with up to 0.33% of TG(20A)C (w/v). Following intravenous bolus injection into rats, TG(20A)C induced a dose-dependent decrease in the serum cholesterol content of maximally 44%, at a dose of 1.9 mg kg-1. This makes TG(20A)C at least 30-fold more effective than the previously developed N-tris-O-(beta-D-galactopyranosyl)methylmethyl-N alpha-4-(5- cholesten-3 beta-yloxy)succinylglycinamide (TG(4A)C), provided with a cluster galactoside that displayed a 2000-fold lower affinity for the asialoglycoprotein receptor than TG(20A). In conclusion, the hypocholesterolemic activity of a cholesterylated galactoside can be strongly enhanced by using a cluster galactoside with higher affinity for the asialoglycoprotein receptor. |
| The cholesterol ester-carrying protein in the transport of saturated fatty acids (a review of the literature) Titov, V. N. (1999), Klin Lab Diagn(5): 3-10. |
| The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. A joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute. The Task Force on Cholesterol Issues, American Heart Association LaRosa, J. C., D. Hunninghake, et al. (1990), Circulation 81(5): 1721-33. |
| The cholesterol granuloma of the frontal sinus. Its radiological morphology and differential diagnostic aspects Zaunbauer, W., C. Fretz, et al. (1992), Rofo 156(5): 497-9. |
| The cholesterol hypothesis has been proved true at last Huttunen, J. (1995), Duodecim 111(5): 385-6. |
| The cholesterol level in the peripheral blood lymphocytes: the interrelationship with ischemic heart disease in patients with different types of hyperlipidemia Bolkhova, L. A., I. V. Fuki, et al. (1993), Biull Eksp Biol Med 116(11): 476-9. Abstract: Variability of cholesterol levels inside lymphocytes (CLL) have been compared with the concentration of total cholesterol, triglycerides and HDL of blood plasma among normal donors and hyperlipidemic patients. Persons with elevated CLL was found among normal donors and hyperlipidemic patients, each group comprising 4-5%. No significant correlation was followed between CLL & the level of total cholesterol, triglyceride & HDL blood plasma level among total observed population. However a consistent correlation was found between CLL & blood plasma cholesterol/triglyceride ratio among patient with elevated plasma triglyceride. |
| The cholesterol lowering effect of antimalarial drugs is enhanced in patients with lupus taking corticosteroid drugs Rahman, P., D. D. Gladman, et al. (1999), J Rheumatol 26(2): 325-30. Abstract: OBJECTIVE: To examine the relationship between antimalarial therapy and total cholesterol in patients with systemic lupus erythematosus (SLE) with or without steroid therapy. METHODS: Retrospective study for the University of Toronto Lupus Clinic database between 1976 and 1997. The effects of antimalarials on random total cholesterol levels were assessed in the following situations: patients not receiving steroids (part I) that either initiated or discontinued antimalarials; patients receiving steroids (part II) that were either on a stable dose or initiating antimalarials; and patients initiating steroids with or without antimalarials (part III). Paired t test, Fisher's exact test, and 2 way analysis of variance were used when appropriate. RESULTS: Initiation of antimalarials reduced the baseline total cholesterol by 4.1 % at 3 months in 53 patients (p = 0.020) and by 0.6% at 6 months in 30 patients (p = NS), while the cessation of antimalarials increased the total cholesterol by 3.6% at 3 months in 38 patients (p = NS) and 5.4% at 6 months in 22 patients (p = NS). In 181 patients taking steroids and antimalarials, the mean total cholesterol was 11% less than for 201 patients receiving a comparable dose of steroids alone (p = 0.0023). Initiation of antimalarials on a stable dose of steroids reduced the total cholesterol by 11.3% at 3 months in 29 patients (p = 0.0002) and 9.4% at 6 months in 20 patients (p = 0.004). For patients initiating steroids, the percentage increase in cholesterol was lower in those taking antimalarials compared to patients without antimalarial therapy (p = 0.0149). CONCLUSION: Antimalarials lower total cholesterol in patients receiving steroids and may minimize steroid induced hypercholesterolemia. |
| The cholesterol membrane anchor of the Hedgehog protein confers stable membrane association to lipid-modified proteins Peters, C., A. Wolf, et al. (2004), Proc Natl Acad Sci U S A 101(23): 8531-6. Abstract: The Hedgehog proteins are potent organizers of animal development. They carry a cholesterol ester at the C terminus of their signaling domain. The membrane anchoring mediated by this lipophilic modification was studied by means of an approach integrating cell biology, biochemistry, biophysics, and organic chemistry techniques. Sterol-modified and fluorescent-labeled Hedgehog-derived peptides and proteins were synthesized and investigated in biophysical and cell-biological assays. These experiments revealed that cholesterol alone anchors proteins to membranes with significant strength and half-times for spontaneous desorption of several hours. Its membrane anchoring ability is comparable to dual lipidation motifs such as double geranylgeranylation or S-palmitoylation plus S-farnesylation found in other lipidated proteins. The experiments also demonstrate that membrane binding changes dramatically if short lipidated peptides are equipped with a large protein. These data suggest that for Hedgehog release and subsequent signaling an interaction partner such as the Dispatched protein is necessary. In addition to these findings the described approach allows one to correlate biophysical data obtained with model peptides with data determined with fully functional proteins and to combine results from in vitro and in vivo experiments. It should be generally applicable to other membrane anchors and proteins. |
| The cholesterol metabolite cholest-4-en-3-one and its 3-oxo derivatives suppress body weight gain, body fat accumulation and serum lipid concentration in mice Suzuki, K., T. Shimizu, et al. (1998), Bioorg Med Chem Lett 8(16): 2133-8. Abstract: Based on the findings that cholest-4-en-3-one, an intestinal metabolite of cholesterol, has an anti-obesity effect on animals, the structure-effect relationship of its 3-oxo derivatives and related compounds were investigated. Cholesten-3-ones, which possesses an enone structure with a carbonyl group at C3, markedly inhibit body weight gain and body fat accumulation, as well as the levels of serum triglyceride and cholesterol in animals without any clinical abnormalities. |
| The cholesterol mobilizing transporter ABCA1 as a new therapeutic target for cardiovascular disease Oram, J. F. (2002), Trends Cardiovasc Med 12(4): 170-5. Abstract: Atherosclerotic cardiovascular disease remains the leading cause of morbidity and mortality in Western societies. A hallmark of the developing atherosclerotic lesion is the appearance of cholesterol-laden macrophages in the artery wall. A cell membrane transporter called ABCA1 mediates the removal of excess cholesterol from macrophages into the lipoprotein pathway. This makes ABCA1 a promising new therapeutic target for reducing cholesterol deposits in tissues, eliminating excess cholesterol from the body, and preventing cardiovascular disease. |