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Hepatic cholesterol 7 alpha-hydroxylase (cytochrome P450 [CYP7A1]) catalyzes the first and rate-limiting step in the bile acid synthetic pathway in humans and rodents. Since bile acids are end products of cholesterol metabolism, we anticipated that changes in CYP7A1 expression might underlie alterations in cholesterol and bile acid homeostasis in transgenic mice overexpressing rat CYP7A1. Transgenic mice were generated with a replication-deficient retroviral vector containing rat CYP7A1 cDNA. After confirmation of CYP7A1 mRNA and protein expression in the liver, serum cholesterol and bile acid levels were evaluated in transgenic and nontransgenic mice. CYP7A1 overexpression increased CYP7A1 expression, increased the amount of Cyp7a1 messenger RNA and protein, and significantly decreased serum cholesterol and bile acid levels. The CYP7A1 transgenic mice had strikingly different serum levels of CYP7A1 mRNA from control animals, which were driven by a relatively insensitive mouse CYP7A1 promoter. Transgenic mice with the relatively insensitive promoter had a greater decrease in total bile acids in the bile, increased accumulation of bile acids and cholesterol in the liver, and decreased nuclear receptor-regulated genes controlling cholesterol and bile acid