Calcium binding by bile acids: in vitro studies using a calcium ion electrode.

In this study, we compared in vitro calcium binding by the taurine and glycine conjugates of the major bile acids in human bile: cholic (CA), chenodeoxycholic (CDCA) and deoxycholic (DCA) acids, together with the cholelitholytic bile acids ursodeoxycholic (UDCA) and ursocholic (UCA) acids. At physio...

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Main Authors: D Gleeson, GM Murphy, RH Dowling
Format: Article
Language:English
Published: Elsevier 1990-05-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520427774
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spelling doaj-ab41ba67ec264a0d916a1c2d8438143b2021-04-25T04:22:46ZengElsevierJournal of Lipid Research0022-22751990-05-01315781791Calcium binding by bile acids: in vitro studies using a calcium ion electrode.D Gleeson0GM Murphy1RH Dowling2Gastroenterology Unit, Guy's Campus, UMDS, Guy's Hospital, London, England.Gastroenterology Unit, Guy's Campus, UMDS, Guy's Hospital, London, England.Gastroenterology Unit, Guy's Campus, UMDS, Guy's Hospital, London, England.In this study, we compared in vitro calcium binding by the taurine and glycine conjugates of the major bile acids in human bile: cholic (CA), chenodeoxycholic (CDCA) and deoxycholic (DCA) acids, together with the cholelitholytic bile acids ursodeoxycholic (UDCA) and ursocholic (UCA) acids. At physiological total calcium (CaTOT) (1-15 mM) and bile acid (BA) (10-50 mM) concentrations, all the bile acids caused concentration-dependent falls in [Ca2+], suggesting calcium binding. Except for glycine-conjugated CDCA, all the other calcium-bile acid complexes were soluble in 150 mM NaCl. The calcium binding affinities followed the pattern: dihydroxy (CDCA, UDCA and DCA) greater than trihydroxy (CA and UCA) bile acids, and glycine conjugates greater than taurine conjugates. The glycine conjugate of UDCA, which increases during UDCA treatment, had the highest calcium binding affinity. Ten-20 mM phospholipid modestly increased calcium binding by CA conjugates, but not by CDCA, UDCA, and DCA conjugates. Phospholipid also prevented the precipitation of glyco-CDCA in the presence of calcium. Bile acid-calcium biding was pH-independent over the range 6.5-8.5. The different calcium binding affinities of the major biliary bile acids may partly explain their varying effects on biliary calcium secretion. The results also suggest that neither precipitation of calcium-bile acid complexes nor impaired calcium binding by bile acids is important in the pathogenesis of human calcium gallstone formation.http://www.sciencedirect.com/science/article/pii/S0022227520427774
collection DOAJ
language English
format Article
sources DOAJ
author D Gleeson
GM Murphy
RH Dowling
spellingShingle D Gleeson
GM Murphy
RH Dowling
Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
Journal of Lipid Research
author_facet D Gleeson
GM Murphy
RH Dowling
author_sort D Gleeson
title Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
title_short Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
title_full Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
title_fullStr Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
title_full_unstemmed Calcium binding by bile acids: in vitro studies using a calcium ion electrode.
title_sort calcium binding by bile acids: in vitro studies using a calcium ion electrode.
publisher Elsevier
series Journal of Lipid Research
issn 0022-2275
publishDate 1990-05-01
description In this study, we compared in vitro calcium binding by the taurine and glycine conjugates of the major bile acids in human bile: cholic (CA), chenodeoxycholic (CDCA) and deoxycholic (DCA) acids, together with the cholelitholytic bile acids ursodeoxycholic (UDCA) and ursocholic (UCA) acids. At physiological total calcium (CaTOT) (1-15 mM) and bile acid (BA) (10-50 mM) concentrations, all the bile acids caused concentration-dependent falls in [Ca2+], suggesting calcium binding. Except for glycine-conjugated CDCA, all the other calcium-bile acid complexes were soluble in 150 mM NaCl. The calcium binding affinities followed the pattern: dihydroxy (CDCA, UDCA and DCA) greater than trihydroxy (CA and UCA) bile acids, and glycine conjugates greater than taurine conjugates. The glycine conjugate of UDCA, which increases during UDCA treatment, had the highest calcium binding affinity. Ten-20 mM phospholipid modestly increased calcium binding by CA conjugates, but not by CDCA, UDCA, and DCA conjugates. Phospholipid also prevented the precipitation of glyco-CDCA in the presence of calcium. Bile acid-calcium biding was pH-independent over the range 6.5-8.5. The different calcium binding affinities of the major biliary bile acids may partly explain their varying effects on biliary calcium secretion. The results also suggest that neither precipitation of calcium-bile acid complexes nor impaired calcium binding by bile acids is important in the pathogenesis of human calcium gallstone formation.
url http://www.sciencedirect.com/science/article/pii/S0022227520427774
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AT rhdowling calciumbindingbybileacidsinvitrostudiesusingacalciumionelectrode
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