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J. Lipid Res.
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A more recent version of this article appeared on May 1, 2003

Papers In Press, published online ahead of print February 16, 2003
J. Lipid Res., doi:10.1194/jlr.M200489-JLR200
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Submitted on December 31, 2002
Revised on February 3, 2003
Accepted on February 4, 2003

Hypercholesterolemia and changes in lipid and bile acid metabolism in male and female CYP7A1 deficient mice

Sandra K. Erickson, Steven R. Lear, Sean Deane, Sandrine Dubrac, Sandra L. Huling, Lien Nguyen, Jaya S. Bollineni, Sarah Shefer, Hideyuki Hyogo, David E. Cohen, Benjamin Shneider, Ephraim Sehayek, Meena Ananthanarayanan, Natarajan Balasubramaniyan, Fredrick J. Suchy, Ashok K. Batta, and Gerald Salen

Medicine Dept., University of California, San Francisco, San Francisco, CA 94121

Corresponding Author: skerick{at}itsa.ucsf.edu

Cholesterol 7a-hydroxylase, a rate-limiting enzyme for bile acid synthesis, has been implicated in genetic susceptibility to atherosclerosis. The gene, CYP7A1, encoding a protein with this activity, is expressed normally only in hepatocytes and is highly regulated. Our cyp7A1 gene knockout mouse colony, as young adults on a chow diet, is hypercholesterolemic. These mice were characterized extensively to understand how cyp7A1 affects lipid and bile acid homeostasis in different tissue compartments and whether gender plays a modifying role. Both male and female cyp7A1 deficient mice had decreased hepatic low density lipoprotein receptors, unchanged hepatic cholesterol synthesis, increased intestinal cholesterol synthesis and bile acid transporters, and decreased fecal bile acids but increased fecal sterols. In females, cyp7A1 deficiency also caused changes in hepatic fatty acid metabolism, decreased hepatic canalicular bile acid transporter, Bsep, and altered gall bladder bile composition to a lithogenic profile. Taken together, the data suggest that cyp7A1 deficiency results in a proatherogenic phenotype in both genders and leads to a prolithogenic phenotype in females.


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