Abstract
Fibric acid derivatives are being used for treatment of hyperlipidemia syndromes for more than 25 years. The drugs markedly lower plasma triglyceride levels, increase HDL cholesterol and have a variable effect on the LDL system. Accordingly, fibrates are considered among the first drugs of choice for patients with type III and type IV hyperlipidemia, are also effective in patients with type V and decrease LDL in some but not all patients with hyperlipidemia types IIA and IIB. The mechanisms responsible for the lipid lowering effects of fibrates are increase of low lipoprotein lipase activity, stimulation of LDL catabolism via receptor-dependent pathway and decreased catabolism of apo A-I the major apoprotein of high density lipoproteins (1). The drugs may also have a direct effect on hepatic lipid metabolism.
Studies carried out in our laboratory during recent years have focused on the effects of one fibric acid analogue — bezafibrate — on the structure, composition and metabolism of lipoproteins in patients with various forms of hyperlipidemia. In addition to the known effects of fibrates on lipoprotein and apoprotein levels, our studies have also elucidated another facet of lipid lowering therapy: correction of abnormal structure and cell metabolism of lipoprotein particles. These data are summarized below, according to the lipoproteins investigated.
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References
Eisenberg S, Gavish D, Kleinman Y.: Bezafibrate. In: Levy RI, Shepherd J, Packard CJ, Miller NE. (eds.). Pharmacological Control of Hyperlipidemia. AR Prous, Barcelona 1986, pp. 145–169.
Weintraub M, Eisenberg S, Breslow JL.: Different patterns of post prandial lipoprotein metabolism in normal, Type IIA, Type III and Type IV hyperlipoproteinemic individuals. Effects of treatment with cholestyramine and gemfibrozil. — Clin Invest 1987;79:1110–1119.
Eisenberg S, Gavish D, Oschry Y, et al.: Abnormalities in very low, low and high density lipoproteins in hypertriglyceridemia. Reversal towards normal with bezafibrate treatment. — Clin Invest 1984; 74: 470–482.
Gavish D, Oschry Y, Fainaru M, et al.: Change in very low-, low-and high-density lipoproteins during lipid lowering (Bezafibrate) therapy. Studies in Type IIA and Type IIB hyperlipoproteinemia. Eur — Clin Invest 1986;16:61–68.
Eisenberg S, Friedman G, Vogel T.: Enhanced metabolism of normolipidemic human plasma very low density lipoprotein in cultured cells by exogenous apolipoprotein E-3. Arteriosclerosis 1988;8:480–487.
Sehayek E, Eisenberg S.: Abnormal composition of hypertriglyceridemic very low density lipoprotein determines abnormal cell metabolism. Arterosclerosis 1988;10:1088–1095.
Kleinman Y, Eisenberg S, Oschry Y, et al.: Defective metabolism of hypertriglyceridemic low density lipoprotein in cultured human skin fibroblasts. — Clin Invest 1985;75:1796–1803.
Kleinman Y, Oschry Y, Eisenberg S.: Abnormal regulation of LDL receptor activity and abnormal cellular metabolism of hypertriglyceridaemic low density lipoprotein. Normalization with bezafibrate therapy. Eur — Clin Invest 1987;17:538–543.
Kleinman Y, Schonfeld G, Gavish D, et al.: Hypolipidemic therapy modulates expression of apolipoprotein — epitopes on low density lipoproteins. Studies in mild to moderate hypertriglyceridemic patients. — Lipid Res 1987;28:540–548.
Eisenberg S.: High density lipoprotein metabolism (JLR Review). — Lipid Res 1984;25:1017–1058.
Brinton EA, Eisenberg S, Breslow JL.: Increased apo A-I and apo A-II fractional catabolic rate in patients with low HDL-cholesterol levels with or without hypertriglyceridemia. — Clin Invest 1991;87: 536–544.
Frick MM, Elo O, Haapa K, et al.: Helsinki Heart Study. Primary prevention trial with gemfibrozil in middle-aged men with dyslipidemia. — Engl — Med 1987;317:1237–1245.
Manninen V, Elo O, Frick MH, et al.: Lipid alternations and decline in the incidence of coronary heart disease in the Helsinki Heart Study. JAMA 1988;260:641–651.
Mahley R, Angelin B.: Type III hyperlipoproteinemia. Recent insights into the genetic defect of familial dysbetalipoproteinemia. Adv Intern Med 1984;29:385–411.
Eisenberg S.: Dyslipoproteinemia and Atherosclerosis. In: Ollson AG (ed). Atherosclerosis, Biology and Clinical Science. Churchill Livingston, 1987 pp. 281–290.
Manninen V, Tekkanen L, Koskinen P, et al.: Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study: Impli cations for treatment. Circulation 1992;85:37–45.
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© 1993 Springer Science+Business Media Dordrecht
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Eisenberg, S. (1993). Effects of Fibrates on the Altered Lipoprotein System in Hypertriglyceridemia. In: Catapano, A.L., Gotto, A.M., Smith, L.C., Paoletti, R. (eds) Drugs Affecting Lipid Metabolism. Medical Science Symposia Series, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1703-6_56
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DOI: https://doi.org/10.1007/978-94-011-1703-6_56
Publisher Name: Springer, Dordrecht
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