AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 264: G1118-G1125, 1993;
0193-1857/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chandler, C. E.
Right arrow Articles by Moberly, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chandler, C. E.
Right arrow Articles by Moberly, J. B.

AJP - Gastrointestinal and Liver Physiology, Vol 264, Issue 6 1118-G1125, Copyright © 1993 by American Physiological Society

ARTICLES

Transepithelial transport of cholyltaurine by Caco-2 cell monolayers is sodium dependent

C. E. Chandler, L. M. Zaccaro and J. B. Moberly
Department of Cardiovascular and Metabolic Diseases, Pfizer Inc., Groton, Connecticut 06340.

Bile acids are efficiently recovered from the intestinal lumen by a Na(+)-dependent transport process that is localized in the ileal enterocyte brush-border membrane. To establish a cell culture model for this process, we examined the Na+ dependence of cholyltaurine (C-tau; taurocholate) transport across monolayers of differentiated Caco-2 cells grown on permeable filter inserts. Transport of [3H]C-tau was Na+ dependent (> 20-fold stimulation), saturable, and time linear for at least 60 min. The apparent Michaelis constant of [3H]C-tau transport was approximately 65 microM, and the maximal transport rate was approximately 800 pmol.min-1.mg protein-1. Transport of [3H]C-tau in the apical-to-basolateral direction was 17-fold greater than transport in the reverse direction. Lowered incubation temperature, various metabolic inhibitors, and various unlabeled bile acids inhibited [3H]C-tau transport. Caco-2 cells thus transport bile acids in a manner similar to that described for ileal brush-border membrane vesicles and isolated ileal enterocytes and are therefore an appropriate model for studying the molecular basis of ileal bile acid transport.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
W. A. Alrefai, Z. Sarwar, S. Tyagi, S. Saksena, P. K. Dudeja, and R. K. Gill
Cholesterol modulates human intestinal sodium-dependent bile acid transporter
Am J Physiol Gastrointest Liver Physiol, May 1, 2005; 288(5): G978 - G985.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
F. Chen, L. Ma, N. Al-Ansari, and B. Shneider
The Role of AP-1 in the Transcriptional Regulation of the Rat Apical Sodium-dependent Bile Acid Transporter
J. Biol. Chem., October 12, 2001; 276(42): 38703 - 38714.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
A.-Q. Sun, I'K. Swaby, S. Xu, and F. J. Suchy
Cell-specific basolateral membrane sorting of the human liver Na+-dependent bile acid cotransporter
Am J Physiol Gastrointest Liver Physiol, June 1, 2001; 280(6): G1305 - G1313.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online