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Abstract
The effect of bezafibrate on HMG-CoA reductase, the key enzyme of cholesterol synthesis, and LDL metabolism was studied in human mononuclear cells. Bezafibrate at concentrations achieved during administration in patients did not suppress preformed reductase in mononuclear cells. Similarly, the drug was ineffective in regulating reductase when added to the medium of cultured cells. Also, the fibrate did not modulate the enzyme suppression mediated by LDL. At very high concentrations bezafibrate enhanced LDL binding, but both total cell association and degradation were unchanged. Thus, the previously observed decrease of HMG-CoA reductase activity in mononuclear cells of patients treated with fibrates is likely to be indirect and probably due to changes in LDL structure.
Published Version
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