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Abstract

Statins, inhibitors of the key enzyme in the endogenous synthesis of cholesterol (3-hydroxy-3-methylglutaryl coenzyme A reductase, or HMG-CoA reductase) have been proven to be very effective in lowering plasma LDL-C levels and significantly reduce the risk of coronary heart disease. Statins also modestly increase plasma levels of HDL-C. The mechanism of the effect of statins on apo A-I metabolism has been studied by several groups. The current literature shows no significant effects of atorvastatin on plasma apo A-I concentrations and apo A-I kinetics, but a significant reduction of both production and clearance of apo A-I with rosuvastatin, without significant changes in plasma apo A-I concentrations. It is thought that the reduction in HDL clearance with rosuvastatin is due to the statin-associated reduction in plasma TG-rich lipoproteins levels, which leads to a reduction in the substrate for cholesteryl ester transfer protein (CETP), and therefore to a reduction in the TG content and increase in cholesterol content of HDL. These results contrast with findings of increased apo A-I expression and production by statins in vitro.

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Correspondence to Stefania Lamon-Fava .

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Lamon-Fava, S. (2010). Effects of Statins on HDL Metabolism. In: Schaefer, E. (eds) High Density Lipoproteins, Dyslipidemia, and Coronary Heart Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1059-2_19

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  • DOI: https://doi.org/10.1007/978-1-4419-1059-2_19

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