Abstract
Clofibrate-induced hypocholesterolemic rats accumulate triparanol-effected desmosterol (24-dehydrocholesterol) no differently than do triparanol-treated normocholesterolemic rats. Accordingly, these findings indicate that hepatic cholesterol biosynthesis proceeds essentially normally in clofibrate-induced hypocholesterolemic rats. Thus, clofibrate-induced hypocholesterolemia is not primarily due to a shutdown of hepatic cholesterol biosynthesis. This conclusion does not exclude the possibility that inhibition of hepatic cholesterol biosynthesis by clofibrate may contribute to some degree to the clofibrate-induced hypocholesterolemia.
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