Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles
Identifieur interne : 000296 ( Istex/Corpus ); précédent : 000295; suivant : 000297Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles
Auteurs : K. J. Van Erpecum ; M. F. J. Stolk ; A. M. W. C. Van Den Broek ; W. Renooij ; B. J. M. Van De Heijning ; G. P. Van Berge HenegouwenSource :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 1993-05.
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- KwdEn :
Abstract
Abstract. Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl‐1 respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: P< 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P<0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.
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DOI: 10.1111/j.1365-2362.1993.tb00775.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title><author><name sortKey="Erpecum, K J Van" sort="Erpecum, K J Van" uniqKey="Erpecum K" first="K. J. Van" last="Erpecum">K. J. Van Erpecum</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Stolk, M F J" sort="Stolk, M F J" uniqKey="Stolk M" first="M. F. J." last="Stolk">M. F. J. Stolk</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Broek, A M W C Van Den" sort="Broek, A M W C Van Den" uniqKey="Broek A" first="A. M. W. C. Van Den" last="Broek">A. M. W. C. Van Den Broek</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Renooij, W" sort="Renooij, W" uniqKey="Renooij W" first="W." last="Renooij">W. Renooij</name><affiliation><mods:affiliation>†Departments of Surgery, University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Heijning, B J M Van De" sort="Heijning, B J M Van De" uniqKey="Heijning B" first="B. J. M. Van De" last="Heijning">B. J. M. Van De Heijning</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Henegouwen, G P Van Berge" sort="Henegouwen, G P Van Berge" uniqKey="Henegouwen G" first="G. P. Van Berge" last="Henegouwen">G. P. Van Berge Henegouwen</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6D842DA0F6AB0E023B3A43142312FC07AEB30E76</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1111/j.1365-2362.1993.tb00775.x</idno><idno type="url">https://api.istex.fr/document/6D842DA0F6AB0E023B3A43142312FC07AEB30E76/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000296</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000296</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title><author><name sortKey="Erpecum, K J Van" sort="Erpecum, K J Van" uniqKey="Erpecum K" first="K. J. Van" last="Erpecum">K. J. Van Erpecum</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Stolk, M F J" sort="Stolk, M F J" uniqKey="Stolk M" first="M. F. J." last="Stolk">M. F. J. Stolk</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Broek, A M W C Van Den" sort="Broek, A M W C Van Den" uniqKey="Broek A" first="A. M. W. C. Van Den" last="Broek">A. M. W. C. Van Den Broek</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Renooij, W" sort="Renooij, W" uniqKey="Renooij W" first="W." last="Renooij">W. Renooij</name><affiliation><mods:affiliation>†Departments of Surgery, University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Heijning, B J M Van De" sort="Heijning, B J M Van De" uniqKey="Heijning B" first="B. J. M. Van De" last="Heijning">B. J. M. Van De Heijning</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Henegouwen, G P Van Berge" sort="Henegouwen, G P Van Berge" uniqKey="Henegouwen G" first="G. P. Van Berge" last="Henegouwen">G. P. Van Berge Henegouwen</name><affiliation><mods:affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Clinical Investigation</title><idno type="ISSN">0014-2972</idno><idno type="eISSN">1365-2362</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1993-05">1993-05</date><biblScope unit="volume">23</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="283">283</biblScope><biblScope unit="page" to="288">288</biblScope></imprint><idno type="ISSN">0014-2972</idno></series><idno type="istex">6D842DA0F6AB0E023B3A43142312FC07AEB30E76</idno><idno type="DOI">10.1111/j.1365-2362.1993.tb00775.x</idno><idno type="ArticleID">ECI283</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bile</term><term>cholesterol</term><term>concentration</term><term>crystals</term><term>nucleation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract. Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl‐1 respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: P< 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P<0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>K. J. VAN ERPECUM</name><affiliations><json:string>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>M. F. J. STOLK</name><affiliations><json:string>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>A. M. W. C. VAN DEN BROEK</name><affiliations><json:string>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>W. RENOOIJβ</name><affiliations><json:string>†Departments of Surgery, University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>B. J. M. VAN DE HEIJNING</name><affiliations><json:string>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>G. P. VAN BERGE HENEGOUWEN</name><affiliations><json:string>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Bile</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cholesterol</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>concentration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>crystals</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>nucleation</value></json:item></subject><articleId><json:string>ECI283</json:string></articleId><language><json:string>eng</json:string></language><abstract>Abstract. Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl‐1 respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: P> 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P>0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.</abstract><qualityIndicators><score>7.074</score><pdfVersion>1.4</pdfVersion><pdfPageSize>601.2 x 793.44 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>2320</abstractCharCount><pdfWordCount>3574</pdfWordCount><pdfCharCount>24636</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>299</abstractWordCount></qualityIndicators><title>Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title><genre><json:string>review-article</json:string></genre><host><volume>23</volume><publisherId><json:string>ECI</json:string></publisherId><pages><total>6</total><last>288</last><first>283</first></pages><issn><json:string>0014-2972</json:string></issn><issue>5</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1365-2362</json:string></eissn><title>European Journal of Clinical Investigation</title><doi><json:string>10.1111/(ISSN)1365-2362</json:string></doi></host><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1111/j.1365-2362.1993.tb00775.x</json:string></doi><id>6D842DA0F6AB0E023B3A43142312FC07AEB30E76</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6D842DA0F6AB0E023B3A43142312FC07AEB30E76/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6D842DA0F6AB0E023B3A43142312FC07AEB30E76/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6D842DA0F6AB0E023B3A43142312FC07AEB30E76/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1993</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title><author><persName><forename type="first">K. J. VAN</forename><surname>ERPECUM</surname></persName><note type="correspondence"><p>Correspondence: Department of Gastroenterology, University Hospital Utrecht, Postbox 85500, 3508 GA Utrecht. The Netherlands.</p></note><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">M. F. J.</forename><surname>STOLK</surname></persName><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">A. M. W. C. VAN DEN</forename><surname>BROEK</surname></persName><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">W.</forename><surname>RENOOIJβ</surname></persName><affiliation>†Departments of Surgery, University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">B. J. M. VAN DE</forename><surname>HEIJNING</surname></persName><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">G. P. VAN BERGE</forename><surname>HENEGOUWEN</surname></persName><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation></author></analytic><monogr><title level="j">European Journal of Clinical Investigation</title><idno type="pISSN">0014-2972</idno><idno type="eISSN">1365-2362</idno><idno type="DOI">10.1111/(ISSN)1365-2362</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1993-05"></date><biblScope unit="volume">23</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="283">283</biblScope><biblScope unit="page" to="288">288</biblScope></imprint></monogr><idno type="istex">6D842DA0F6AB0E023B3A43142312FC07AEB30E76</idno><idno type="DOI">10.1111/j.1365-2362.1993.tb00775.x</idno><idno type="ArticleID">ECI283</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract. Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl‐1 respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: P< 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P<0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Bile</term></item><item><term>cholesterol</term></item><item><term>concentration</term></item><item><term>crystals</term></item><item><term>nucleation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6D842DA0F6AB0E023B3A43142312FC07AEB30E76/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2362</doi><issn type="print">0014-2972</issn><issn type="electronic">1365-2362</issn><idGroup><id type="product" value="ECI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF CLINICAL INVESTIGATION">European Journal of Clinical Investigation</title></titleGroup></publicationMeta><publicationMeta level="part" position="05005"><doi origin="wiley">10.1111/eci.1993.23.issue-5</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="1993-05">May 1993</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="0028300" status="forIssue"><doi origin="wiley">10.1111/j.1365-2362.1993.tb00775.x</doi><idGroup><id type="unit" value="ECI283"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Review</title></titleGroup><eventGroup><event type="firstOnline" date="2008-03-20"></event><event type="publishedOnlineFinalForm" date="2008-03-20"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-20"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-20"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="283">283</numbering><numbering type="pageLast" number="288">288</numbering></numberingGroup><correspondenceTo>Department of Gastroenterology, University Hospital Utrecht, Postbox 85500, 3508 GA Utrecht. The Netherlands.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ECI.ECI283.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 9 July 1992 and in revised form 7 January 1993; accepted 12 January 1993</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="34"></count><count type="linksCrossRef" number="7"></count></countGroup><titleGroup><title type="main">Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>K. J. VAN</givenNames><familyName>ERPECUM</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>M. F. J.</givenNames><familyName>STOLK</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>A. M. W. C. VAN DEN</givenNames><familyName>BROEK</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>W.</givenNames><familyName>RENOOIJβ</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>B. J. M. VAN DE</givenNames><familyName>HEIJNING</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>G. P. VAN BERGE</givenNames><familyName>HENEGOUWEN</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="NL"><unparsedAffiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="NL"><unparsedAffiliation>†Departments of Surgery, University Hospital Utrecht, The Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Bile</keyword><keyword xml:id="k2">cholesterol</keyword><keyword xml:id="k3">concentration</keyword><keyword xml:id="k4">crystals</keyword><keyword xml:id="k5">nucleation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Abstract. </b> Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl<sup>‐1</sup> respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: <i>P<</i> 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P<0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Bile concentration promotes nucleation of cholesterol monohydrate crystals by increasing the cholesterol concentration in the vesicles</title></titleInfo><name type="personal"><namePart type="given">K. J. VAN</namePart><namePart type="family">ERPECUM</namePart><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation><description>Correspondence: Department of Gastroenterology, University Hospital Utrecht, Postbox 85500, 3508 GA Utrecht. The Netherlands.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. F. J.</namePart><namePart type="family">STOLK</namePart><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. M. W. C. VAN DEN</namePart><namePart type="family">BROEK</namePart><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">RENOOIJβ</namePart><affiliation>†Departments of Surgery, University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. J. M. VAN DE</namePart><namePart type="family">HEIJNING</namePart><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. P. VAN BERGE</namePart><namePart type="family">HENEGOUWEN</namePart><affiliation>*Departments of Gastroenterology and University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1993-05</dateIssued><edition>Received 9 July 1992 and in revised form 7 January 1993; accepted 12 January 1993</edition><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">34</extent></physicalDescription><abstract lang="en">Abstract. Cholesterol in bile is solubilized in mixed micelles and cholesterol‐phospholipid vesicles. Biliary cholesterol supersaturation and increased concentration of bile in the gallbladder promotes nucleation of cholesterol monohydrate crystals and gallstone formation, possibly by creating unstable vesicles with a high cholesterol/phospholipid ratio. In the present study super‐saturated and unsaturated biles (cholesterol saturation index (CSI) 1.4 and 0.8 respectively) were prepared with concentrations typical of gallbladder and more dilute hepatic bile (total lipid concentration (TLCo) 10 and 2.5 g dl‐1 respectively). The distribution of cholesterol between vesicles and micelles, and vesicular cholesterol/phospholipid ratio were studied using ultracentrifugation and gel‐permeation chromatography. The nucleation time of cholesterol crystals was determined in whole model bile, and in the vesicular and micellar peak fractions. Increased CSI and bile dilution led to an increased proportion of cholesterol solubilized in vesicles. The concentration of bile did not influence vesicular cholesterol/phospholipid ratio. The vesicular cholesterol/ phospholipid ratio found in gel‐permeation chromatography experiments was similar at high and low CSI, whereas the ratio was significantly higher in supersaturated than in unsaturated biles in ultracentrifugation studies. Nucleation of cholesterol crystals from whole model bile was more rapid at the higher bile concentration and higher cholesterol saturation. Nucleation time in whole model bile correlated significantly with nucleation time in the corresponding vesicular peak fraction obtained by gel‐permeation chromatography (r = 0,58: P< 0.01) and with the cholesterol concentration in this vesicular peak (r= ‐0.77; P<0.002) but not with vesicular peak cholesterol/phospholipid ratio. Highest vesicular peak cholesterol concentrations and shortest nucleation times were found for concentrated supersaturated biles, whereas vesicular cholesterol/phospholipid ratio was not different from dilute or unsaturated biles. The present study indicates that increased concentration of bile promotes nucleation of cholesterol crystals by increasing the concentration of cholesterol in the vesicular peak rather than by changing its cholesterol/phospholipid ratio.</abstract><subject lang="en"><genre>Keywords</genre><topic>Bile</topic><topic>cholesterol</topic><topic>concentration</topic><topic>crystals</topic><topic>nucleation</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Clinical Investigation</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0014-2972</identifier><identifier type="eISSN">1365-2362</identifier><identifier type="DOI">10.1111/(ISSN)1365-2362</identifier><identifier type="PublisherID">ECI</identifier><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>283</start><end>288</end><total>6</total></extent></part></relatedItem><identifier type="istex">6D842DA0F6AB0E023B3A43142312FC07AEB30E76</identifier><identifier type="DOI">10.1111/j.1365-2362.1993.tb00775.x</identifier><identifier type="ArticleID">ECI283</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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