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Articles in PresS, published online ahead of print February 19, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00363.2001
Submitted on August 9, 2001
Accepted on February 6, 2002
1 Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan
2 Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Tokyo, Japan
3 Division of Clinical Pharmacology and Toxicology, Department of Medicine, University Hospital, Zurich, Switzerland
* To whom correspondence should be addressed. E-mail: sugiyama{at}mol.f.u-tokyo.ac.jp.
The gender difference in the urinary excretion of estradiol-17ß-glucuronide (E2-17ßG) was examined in rats. The urinary clearance of E2-17ßG was more than 250 times lower in male than in female rats. No such major gender difference was observed in its biliary excretion or metabolism in kidney homogenate. Both the plasma protein binding and inulin clearance were comparable in male and female rats, suggesting that this gender difference cannot be explained by glomerular filtration. The urinary clearance with respect to the plasma unbound E2-17ßG in male rats was less than 1% of the glomerular filtration rate, indicating its potential reabsorption by the kidney and this increased to a level comparable with that found in female rats when dibromosulfophthalein was coinfused. A marked increase in E2-17ßG urinary excretion was also observed in male rats that had undergone orchidectomy. Testosterone injections given to female rats reduced the urinary excretion to a level comparable with control male rats. The concomitant change in the expression of the gene product for organic anion transporting polypeptide Oatp1, of which E2-17ßG is a typical substrate, was found in the kidney membrane fractions following these treatments. These results suggest that urinary E2-17ßG excretion is subject to hormonal regulation and the large gender difference can be explained by that in Oatp1-mediated reabsorption.
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