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Review [Plant sterols and stanols] 2007
Puspa J, Klör HU. · Institut für Betriebslehre der Agrar- und Ernährungswirtschaft der Justus-Liebig-Universität, Giessen, Germany. · Ther Umsch. · Pubmed #17323287 No free full text.
Abstract: Plant sterols and stanols are similar in chemical structure to cholesterol, differing in their side chain configuration. The mechanism by which they lower cholesterol is thought to involve inhibition of cholesterol absorption. A number of products containing plant sterols are now available. A limitation on the development of such products is the poor water solubility of plant sterols. The most common solution is to esterify plant stanols or sterols with fatty acids to enhance availability in food fats such as margarines and salad dressings. A number of studies have shown the efficacy of plant stanol- and sterol-enriched margarines for lowering cholesterol. However, there have been no studies demonstrating that consumption of these stanol ester-containing margarines influences the incidence of coronary heart disease.
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Clinical Conference Effects of fluvastatin on biliary lipids in subjects with an elevated cholesterol saturation index. 2001
Porsch-Ozçürümez M, Hardt PD, Schnell-Kretschmer H, von Bergmann K, Darui C, Nonhoff J, Abletshauser C, Klör HU. · Universitätsklinikum Regensburg, Institut für Klinische Chemie und Blutbank, Franz-Josef-Strauss-Allee 11, D-93053 Regensburg, Germany. · Eur J Clin Pharmacol. · Pubmed #11317474 No free full text.
Abstract: OBJECTIVE: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors have been suggested as agents to reduce the biliary cholesterol saturation index (CSI) in duodenal bile and therefore might be supportive in primary or secondary prevention of gallstones. However, the efficiency of the therapy seems to depend on both the HMG-CoA reductase inhibitor used and the study population selected. METHODS: We therefore investigated the effect of a high-dose application of fluvastatin on biliary lipid composition in 21 subjects exhibiting mild hypercholesterolaemia and a history of current gallstones or cholecystectomy due to gallstone disease. Subjects were treated either with 40 mg fluvastatin twice per day over a 3-month period (n = 14) or with placebo (n = 7). Bile samples were aspirated during endoscopy after intravenous ceruletid stimulation before and after therapy. RESULTS: Both groups were comparable in CSI (mean +/- SD) at baseline (1.78 +/- 0.2 placebo vs. 1.97 +/- 0.4 verum). CSI significantly decreased in the verum group to 1.45 +/- 0.4 (P = 0.003) mainly due to increased phospholipid levels, whereas no difference was observed in the placebo group (1.85 +/- 0.7, n.s.). In addition, the verum group exhibited a significant reduction of hydrophobic deoxycholic acid, which has been reported to induce cholesterol crystal precipitation, and an increase of hydrophilic cholic acid. CONCLUSION: Fluvastatin might decrease the risk of cholesterol gallstone formation in patients with elevated biliary CSI during long-term treatment by reduction of biliary cholesterol saturation and percentage change in deoxycholic acid content.
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