Journal of Lipid Research, Vol 34, 915-921, Copyright © 1993 by Lipid Research, Inc.
Metabolism and choleretic activity of homochenodeoxycholic acid in the hamster
S Miki, BI Cohen, T Mikami and EH Mosbach
Department of Surgery, Beth Israel Medical Center, New York, NY 10003.
The hepatic metabolism and the choleretic effect of homochenodeoxycholic
acid, the C25 homologue of chenodeoxycholic acid, were investigated in the
hamster. After intravenous administration of 3H-labeled
homochenodeoxycholic acid into biliary fistula hamsters, more than 80% of
the radioactivity was recovered in bile in 4 h. A relatively small
proportion of homochenodeoxycholic acid was present in bile as the taurine
(22%) or glycine (4%) conjugate. However, more than 70% of the administered
compound was biotransformed into C23 bile acids. The major C23 metabolites
in bile were norchenodeoxycholic acid (17%), tauronorchenodeoxycholic acid
(33%), and a trihydroxy norbile acid (identified as 3 alpha, 5 beta, 7
alpha-trihydroxy-24-nor-5 beta- cholan-23-oic acid, 19%). Small amounts
(< 5%) of sulfate(s) and glucuronide(s) were also detected.
Homochenodeoxycholic acid, when infused intravenously into the hamster,
produced a striking choleresis. The increase in bile flow after infusion of
this compound was 6- to 7- times that induced by chenodeoxycholic acid. The
apparent choleretic activity of homochenodeoxycholic acid, 181
microliters/mumol, was much greater than that of chenodeoxycholic acid, 11
microliters/mumol. In conclusion, homochenodeoxycholic acid induced a
hypercholeresis of the same order of magnitude as norchenodeoxycholic acid,
presumably because considerable proportions of this compound were degraded
to the hypercholeretic norchenodeoxycholic acid via beta-oxidation in the
liver.
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