Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones
Identifieur interne : 000A98 ( Istex/Corpus ); précédent : 000A97; suivant : 000A99Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones
Auteurs : Jeffery L. Smith ; Paul D. Roach ; Leonie N. Wittenberg ; Michel Riottot ; S. Praga Pillay ; Paul J. Nestel ; Les K. NathansonSource :
- Journal of Gastroenterology and Hepatology [ 0815-9319 ] ; 2000-08.
English descriptors
- KwdEn :
- Acat, Bile, Bile acid hydrophobicity, Bile acid synthesis, Bile acids, Bile lithogenicity, Bile samples, Biliary, Biliary lipid secretion, Biliary lipids, Bladder, Chenodeoxycholic, Chenodeoxycholic acid, Choleretic effect, Cholesterol, Cholesterol acyltransferase, Cholesterol gallstones, Cholesterol metabolism, Cholesterol saturation index, Cholesterol synthesis, Collection times, Common bile duct, Control group, Control patients, Density lipoprotein, Density lipoprotein receptor, Dihydroxylated trihydroxylated bile acids, Gall bladder, Gallbladder bile, Gallstone, Gallstone patients, Hepatic, Hepatic acat activity, Hepatic cholesterol metabolism, Hepatology, Hydrophobicity, Hydrophobicity index, Inhibitor, Intestinal absorption, Lathosterol, Lipid, Lipid concentrations, Lipoprotein, Lithogenic, Lithogenic index, Lithogenicity, Liver biopsies, Liver samples, Metabolism, Mononuclear, Mononuclear cells, Natl acad, Plasma cholesterol, Plasma lathosterol cholesterol, Pravastatin, Present study, Receptor, Receptor activity, Receptor protein, Reductase, Reductase inhibitor, Reductase inhibitors, Simvastatin, Simvastatin administration, Simvastatin group, Simvastatin treatment, Ursodeoxycholic, Ursodeoxycholic acid.
- Teeft :
- Acat, Bile, Bile acid hydrophobicity, Bile acid synthesis, Bile acids, Bile lithogenicity, Bile samples, Biliary, Biliary lipid secretion, Biliary lipids, Bladder, Chenodeoxycholic, Chenodeoxycholic acid, Choleretic effect, Cholesterol, Cholesterol acyltransferase, Cholesterol gallstones, Cholesterol metabolism, Cholesterol saturation index, Cholesterol synthesis, Collection times, Common bile duct, Control group, Control patients, Density lipoprotein, Density lipoprotein receptor, Dihydroxylated trihydroxylated bile acids, Gall bladder, Gallbladder bile, Gallstone, Gallstone patients, Hepatic, Hepatic acat activity, Hepatic cholesterol metabolism, Hepatology, Hydrophobicity, Hydrophobicity index, Inhibitor, Intestinal absorption, Lathosterol, Lipid, Lipid concentrations, Lipoprotein, Lithogenic, Lithogenic index, Lithogenicity, Liver biopsies, Liver samples, Metabolism, Mononuclear, Mononuclear cells, Natl acad, Plasma cholesterol, Plasma lathosterol cholesterol, Pravastatin, Present study, Receptor, Receptor activity, Receptor protein, Reductase, Reductase inhibitor, Reductase inhibitors, Simvastatin, Simvastatin administration, Simvastatin group, Simvastatin treatment, Ursodeoxycholic, Ursodeoxycholic acid.
Abstract
Background and Aims : There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.
Url:
DOI: 10.1046/j.1440-1746.2000.02231.x
Links to Exploration step
ISTEX:3AD559DE21C323983721B84AE422CB10BCD756B8Le document en format XML
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Roach</name><affiliation><mods:affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</mods:affiliation></affiliation></author><author><name sortKey="Wittenberg, Leonie N" sort="Wittenberg, Leonie N" uniqKey="Wittenberg L" first="Leonie N" last="Wittenberg">Leonie N. Wittenberg</name><affiliation><mods:affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</mods:affiliation></affiliation></author><author><name sortKey="Riottot, Michel" sort="Riottot, Michel" uniqKey="Riottot M" first="Michel" last="Riottot">Michel Riottot</name><affiliation><mods:affiliation>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.</mods:affiliation></affiliation></author><author><name sortKey="Pillay, S Praga" sort="Pillay, S Praga" uniqKey="Pillay S" first="S. Praga" last="Pillay">S. 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Smith</name><affiliation><mods:affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</mods:affiliation></affiliation></author><author><name sortKey="Roach, Paul D" sort="Roach, Paul D" uniqKey="Roach P" first="Paul D" last="Roach">Paul D. Roach</name><affiliation><mods:affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</mods:affiliation></affiliation></author><author><name sortKey="Wittenberg, Leonie N" sort="Wittenberg, Leonie N" uniqKey="Wittenberg L" first="Leonie N" last="Wittenberg">Leonie N. Wittenberg</name><affiliation><mods:affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</mods:affiliation></affiliation></author><author><name sortKey="Riottot, Michel" sort="Riottot, Michel" uniqKey="Riottot M" first="Michel" last="Riottot">Michel Riottot</name><affiliation><mods:affiliation>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.</mods:affiliation></affiliation></author><author><name sortKey="Pillay, S Praga" sort="Pillay, S Praga" uniqKey="Pillay S" first="S. Praga" last="Pillay">S. Praga Pillay</name><affiliation><mods:affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</mods:affiliation></affiliation></author><author><name sortKey="Nestel, Paul J" sort="Nestel, Paul J" uniqKey="Nestel P" first="Paul J" last="Nestel">Paul J. Nestel</name><affiliation><mods:affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</mods:affiliation></affiliation></author><author><name sortKey="Nathanson, Les K" sort="Nathanson, Les K" uniqKey="Nathanson L" first="Les K" last="Nathanson">Les K. Nathanson</name><affiliation><mods:affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Gastroenterology and Hepatology</title><title level="j" type="alt">JOURNAL OF GASTROENTEROLOGY HEPATOLOGY</title><idno type="ISSN">0815-9319</idno><idno type="eISSN">1440-1746</idno><imprint><biblScope unit="vol">15</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="871">871</biblScope><biblScope unit="page" to="879">879</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2000-08">2000-08</date></imprint><idno type="ISSN">0815-9319</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0815-9319</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acat</term><term>Bile</term><term>Bile acid hydrophobicity</term><term>Bile acid synthesis</term><term>Bile acids</term><term>Bile lithogenicity</term><term>Bile samples</term><term>Biliary</term><term>Biliary lipid secretion</term><term>Biliary lipids</term><term>Bladder</term><term>Chenodeoxycholic</term><term>Chenodeoxycholic acid</term><term>Choleretic effect</term><term>Cholesterol</term><term>Cholesterol acyltransferase</term><term>Cholesterol gallstones</term><term>Cholesterol metabolism</term><term>Cholesterol saturation index</term><term>Cholesterol synthesis</term><term>Collection times</term><term>Common bile duct</term><term>Control group</term><term>Control patients</term><term>Density lipoprotein</term><term>Density lipoprotein receptor</term><term>Dihydroxylated trihydroxylated bile acids</term><term>Gall bladder</term><term>Gallbladder bile</term><term>Gallstone</term><term>Gallstone patients</term><term>Hepatic</term><term>Hepatic acat activity</term><term>Hepatic cholesterol metabolism</term><term>Hepatology</term><term>Hydrophobicity</term><term>Hydrophobicity index</term><term>Inhibitor</term><term>Intestinal absorption</term><term>Lathosterol</term><term>Lipid</term><term>Lipid concentrations</term><term>Lipoprotein</term><term>Lithogenic</term><term>Lithogenic index</term><term>Lithogenicity</term><term>Liver biopsies</term><term>Liver samples</term><term>Metabolism</term><term>Mononuclear</term><term>Mononuclear cells</term><term>Natl acad</term><term>Plasma cholesterol</term><term>Plasma lathosterol cholesterol</term><term>Pravastatin</term><term>Present study</term><term>Receptor</term><term>Receptor activity</term><term>Receptor protein</term><term>Reductase</term><term>Reductase inhibitor</term><term>Reductase inhibitors</term><term>Simvastatin</term><term>Simvastatin administration</term><term>Simvastatin group</term><term>Simvastatin treatment</term><term>Ursodeoxycholic</term><term>Ursodeoxycholic acid</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Acat</term><term>Bile</term><term>Bile acid hydrophobicity</term><term>Bile acid synthesis</term><term>Bile acids</term><term>Bile lithogenicity</term><term>Bile samples</term><term>Biliary</term><term>Biliary lipid secretion</term><term>Biliary lipids</term><term>Bladder</term><term>Chenodeoxycholic</term><term>Chenodeoxycholic acid</term><term>Choleretic effect</term><term>Cholesterol</term><term>Cholesterol acyltransferase</term><term>Cholesterol gallstones</term><term>Cholesterol metabolism</term><term>Cholesterol saturation index</term><term>Cholesterol synthesis</term><term>Collection times</term><term>Common bile duct</term><term>Control group</term><term>Control patients</term><term>Density lipoprotein</term><term>Density lipoprotein receptor</term><term>Dihydroxylated trihydroxylated bile acids</term><term>Gall bladder</term><term>Gallbladder bile</term><term>Gallstone</term><term>Gallstone patients</term><term>Hepatic</term><term>Hepatic acat activity</term><term>Hepatic cholesterol metabolism</term><term>Hepatology</term><term>Hydrophobicity</term><term>Hydrophobicity index</term><term>Inhibitor</term><term>Intestinal absorption</term><term>Lathosterol</term><term>Lipid</term><term>Lipid concentrations</term><term>Lipoprotein</term><term>Lithogenic</term><term>Lithogenic index</term><term>Lithogenicity</term><term>Liver biopsies</term><term>Liver samples</term><term>Metabolism</term><term>Mononuclear</term><term>Mononuclear cells</term><term>Natl acad</term><term>Plasma cholesterol</term><term>Plasma lathosterol cholesterol</term><term>Pravastatin</term><term>Present study</term><term>Receptor</term><term>Receptor activity</term><term>Receptor protein</term><term>Reductase</term><term>Reductase inhibitor</term><term>Reductase inhibitors</term><term>Simvastatin</term><term>Simvastatin administration</term><term>Simvastatin group</term><term>Simvastatin treatment</term><term>Ursodeoxycholic</term><term>Ursodeoxycholic acid</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Background and Aims : There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>simvastatin</json:string><json:string>lipid</json:string><json:string>hepatic</json:string><json:string>receptor</json:string><json:string>lipoprotein</json:string><json:string>biliary</json:string><json:string>reductase</json:string><json:string>gallstone</json:string><json:string>hydrophobicity</json:string><json:string>cholesterol synthesis</json:string><json:string>bile</json:string><json:string>lithogenic</json:string><json:string>acat</json:string><json:string>lithogenicity</json:string><json:string>ursodeoxycholic</json:string><json:string>pravastatin</json:string><json:string>bile lithogenicity</json:string><json:string>bladder</json:string><json:string>mononuclear cells</json:string><json:string>chenodeoxycholic</json:string><json:string>bile acid hydrophobicity</json:string><json:string>hepatology</json:string><json:string>lathosterol</json:string><json:string>receptor activity</json:string><json:string>simvastatin group</json:string><json:string>hepatic cholesterol metabolism</json:string><json:string>metabolism</json:string><json:string>receptor protein</json:string><json:string>gall bladder</json:string><json:string>ursodeoxycholic acid</json:string><json:string>chenodeoxycholic acid</json:string><json:string>simvastatin administration</json:string><json:string>gallstone patients</json:string><json:string>present study</json:string><json:string>plasma cholesterol</json:string><json:string>plasma lathosterol cholesterol</json:string><json:string>reductase inhibitors</json:string><json:string>hydrophobicity index</json:string><json:string>control group</json:string><json:string>control patients</json:string><json:string>cholesterol acyltransferase</json:string><json:string>bile acids</json:string><json:string>simvastatin treatment</json:string><json:string>biliary lipid secretion</json:string><json:string>bile acid synthesis</json:string><json:string>mononuclear</json:string><json:string>gallbladder bile</json:string><json:string>choleretic effect</json:string><json:string>lipid concentrations</json:string><json:string>bile samples</json:string><json:string>biliary lipids</json:string><json:string>density lipoprotein receptor</json:string><json:string>intestinal absorption</json:string><json:string>hepatic acat activity</json:string><json:string>lithogenic index</json:string><json:string>cholesterol gallstones</json:string><json:string>density lipoprotein</json:string><json:string>common bile duct</json:string><json:string>reductase inhibitor</json:string><json:string>natl acad</json:string><json:string>dihydroxylated trihydroxylated bile acids</json:string><json:string>collection times</json:string><json:string>liver biopsies</json:string><json:string>cholesterol saturation index</json:string><json:string>cholesterol metabolism</json:string><json:string>liver samples</json:string><json:string>cholesterol</json:string><json:string>inhibitor</json:string></teeft></keywords><author><json:item><name>Jeffery L Smith</name><affiliations><json:string>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</json:string></affiliations></json:item><json:item><name>Paul D Roach</name><affiliations><json:string>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</json:string></affiliations></json:item><json:item><name>Leonie N Wittenberg</name><affiliations><json:string>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</json:string></affiliations></json:item><json:item><name>Michel Riottot</name><affiliations><json:string>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.</json:string></affiliations></json:item><json:item><name>S. Praga Pillay</name><affiliations><json:string>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</json:string></affiliations></json:item><json:item><name>Paul J Nestel</name><affiliations><json:string>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</json:string></affiliations></json:item><json:item><name>Les K Nathanson</name><affiliations><json:string>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>biliary lipids</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>choleretic</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>low density lipoprotein receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lithogenic index</value></json:item></subject><articleId><json:string>JGH2231</json:string></articleId><arkIstex>ark:/67375/WNG-N414FV0X-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background and Aims : There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.</abstract><qualityIndicators><score>7.684</score><pdfWordCount>5482</pdfWordCount><pdfCharCount>36169</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595 x 779 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>57</abstractWordCount><abstractCharCount>401</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title><pmid><json:string>11022827</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Gastroenterology and Hepatology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1440-1746</json:string></doi><issn><json:string>0815-9319</json:string></issn><eissn><json:string>1440-1746</json:string></eissn><publisherId><json:string>JGH</json:string></publisherId><volume>15</volume><issue>8</issue><pages><first>871</first><last>879</last><total>9</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2000</json:string><json:string>9/3/1</json:string></date><geogName></geogName><orgName><json:string>Department of Surgery</json:string><json:string>Division of Health Sciences</json:string><json:string>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, QLD</json:string><json:string>University of Queensland</json:string><json:string>Amersham Laboratories</json:string><json:string>Australia and USA</json:string><json:string>Randox Laboratories</json:string><json:string>Blackwell Science Asia Pty</json:string><json:string>Crumlin, Co</json:string><json:string>Varian Associates Inc</json:string><json:string>South Australia, Australia</json:string><json:string>Bio-Rad Laboratories</json:string><json:string>Scandinavian Simvastatin Survival Study Group.</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Mini Protean</json:string><json:string>Mervyn Neely</json:string><json:string>Mike Franklin</json:string><json:string>Bequest Fund</json:string><json:string>David Colquhoun</json:string><json:string>Plasma</json:string><json:string>Table</json:string><json:string>Neil Walker</json:string><json:string>Samples</json:string><json:string>Alan Clague</json:string><json:string>Michel Parquet</json:string><json:string>Associate Professor</json:string><json:string>Scott Moody</json:string><json:string>Calliope Trianta</json:string></persName><placeName><json:string>Brisbane</json:string><json:string>Australia</json:string><json:string>UK</json:string><json:string>USA</json:string><json:string>CA</json:string><json:string>France</json:string><json:string>Harbor City</json:string><json:string>Hercules</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Watts et al.</json:string><json:string>Folch et al.</json:string><json:string>Smith et al.</json:string><json:string>Gastroenterology and Hepatology (2000)</json:string><json:string>Reihnér et al.</json:string><json:string>Roach et al.</json:string><json:string>Arad et al.</json:string><json:string>Strasberg et al.</json:string><json:string>Kwok et al.</json:string><json:string>Lowry et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-N414FV0X-J</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - gastroenterology & hepatology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - gastroenterology & hepatology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Gastroenterology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Hepatology</json:string></scopus></categories><publicationDate>2000</publicationDate><copyrightDate>2000</copyrightDate><doi><json:string>10.1046/j.1440-1746.2000.02231.x</json:string></doi><id>3AD559DE21C323983721B84AE422CB10BCD756B8</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/3AD559DE21C323983721B84AE422CB10BCD756B8/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/3AD559DE21C323983721B84AE422CB10BCD756B8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3AD559DE21C323983721B84AE422CB10BCD756B8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2000-08"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title><title level="a" type="short">Simvastatin and gallstone patients</title><author xml:id="author-0000"><persName><forename type="first">Jeffery L</forename><surname>Smith</surname></persName><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Paul D</forename><surname>Roach</surname></persName><affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Leonie N</forename><surname>Wittenberg</surname></persName><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Michel</forename><surname>Riottot</surname></persName><affiliation>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.<address><country key="FR"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">S. Praga</forename><surname>Pillay</surname></persName><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Paul J</forename><surname>Nestel</surname></persName><affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Les K</forename><surname>Nathanson</surname></persName><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,<address><country key="AU"></country></address></affiliation></author><idno type="istex">3AD559DE21C323983721B84AE422CB10BCD756B8</idno><idno type="ark">ark:/67375/WNG-N414FV0X-J</idno><idno type="DOI">10.1046/j.1440-1746.2000.02231.x</idno><idno type="unit">JGH2231</idno><idno type="toTypesetVersion">file:JGH.JGH2231.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Gastroenterology and Hepatology</title><title level="j" type="alt">JOURNAL OF GASTROENTEROLOGY HEPATOLOGY</title><idno type="pISSN">0815-9319</idno><idno type="eISSN">1440-1746</idno><idno type="book-DOI">10.1111/(ISSN)1440-1746</idno><idno type="book-part-DOI">10.1111/jgh.2000.15.issue-8</idno><idno type="product">JGH</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">15</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="871">871</biblScope><biblScope unit="page" to="879">879</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2000-08"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>
<hi rend="bold"><hi rend="italic">Background and Aims</hi></hi>: There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.</p><p>
<hi rend="bold"><hi rend="italic">Methods</hi></hi>: Thirty‐one gallstone patients were enrolled in the study; 17 were treated with 20 mg simvastatin daily for 3 weeks prior to cholecystectomy and 14 served as controls. Samples of blood, liver, gall‐bladder bile and bile from the common bile duct (CBD) were collected and analysed.</p><p>
<hi rend="bold"><hi rend="italic">Results</hi></hi>: The plasma cholesterol (−30%), triacylglycerol (−23%) and low‐density lipoprotein (LDL) cholesterol (−42%) concentrations were significantly lowered by simvastatin treatment, as was the plasma lathosterol : cholesterol (−70%), which reflects whole‐body cholesterol synthesis. Despite these changes, the hepatic LDL receptor protein and LDL receptor activity in circulating mononuclear cells were similar in both groups. There were no differences in the plasma phytosterol : cholesterol, which reflects the intestinal cholesterol absorption capacity or in the activity of hepatic acyl‐coenzyme A : cholesterol acyltransferase. There were however, lower cholesterol concentrations in CBD (−68%) and gall bladder (−41%) bile, and decreased lithogenic (−47%) and bile acid hydrophobicity (−22%) indices of CBD bile in the simvastatin group.</p><p>
<hi rend="bold"><hi rend="italic">Conclusions</hi></hi>: These data indicate that simvastatin reduced plasma and biliary cholesterol levels primarily by reducing cholesterol synthesis. The reduction in CBD bile lithogenicity and bile acid hydrophobicity by simvastatin suggests that this agent may be useful for people who have early stages of cholesterol gallstone development and in whom a choleretic effect is required.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">biliary lipids</term><term xml:id="k2">choleretic</term><term xml:id="k3">3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors</term><term xml:id="k4">low density lipoprotein receptor</term><term xml:id="k5">lithogenic index</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/3AD559DE21C323983721B84AE422CB10BCD756B8/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 Science Pty</publisherName><publisherLoc>Melbourne, Australia</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1746</doi><issn type="print">0815-9319</issn><issn type="electronic">1440-1746</issn><idGroup><id type="product" value="JGH"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF GASTROENTEROLOGY HEPATOLOGY">Journal of Gastroenterology and Hepatology</title></titleGroup></publicationMeta><publicationMeta level="part" position="08008"><doi origin="wiley">10.1111/jgh.2000.15.issue-8</doi><numberingGroup><numbering type="journalVolume" number="15">15</numbering><numbering type="journalIssue" number="8">8</numbering></numberingGroup><coverDate startDate="2000-08">August 2000</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0087100" status="forIssue"><doi origin="wiley">10.1046/j.1440-1746.2000.02231.x</doi><idGroup><id type="unit" value="JGH2231"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2001-12-25"></event><event type="publishedOnlineFinalForm" date="2001-12-25"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.4 mode:FullText source:Header result:Header" date="2010-03-30"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="871">871</numbering><numbering type="pageLast" number="879">879</numbering></numberingGroup><correspondenceTo> Dr Jl Smith, Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, QLD 4029 Australia. Email:
<email>J.Smith@mailbox.uq.edu.au</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JGH.JGH2231.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="6"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="52"></count><count type="wordTotal" number="6383"></count><count type="linksPubMed" number="44"></count><count type="linksCrossRef" number="1"></count></countGroup><titleGroup><title type="main">Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title><title type="shortAuthors">JL Smith <i>et al.</i></title><title type="short">Simvastatin and gallstone patients</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Jeffery L</givenNames><familyName>Smith</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Paul D</givenNames><familyName>Roach</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Leonie N</givenNames><familyName>Wittenberg</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>Michel</givenNames><familyName>Riottot</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>S. Praga</givenNames><familyName>Pillay</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>Paul J</givenNames><familyName>Nestel</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Les K</givenNames><familyName>Nathanson</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="AU"><unparsedAffiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="AU"><unparsedAffiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">biliary lipids</keyword><keyword xml:id="k2">choleretic</keyword><keyword xml:id="k3">3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors</keyword><keyword xml:id="k4">low density lipoprotein receptor</keyword><keyword xml:id="k5">lithogenic index</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p> <b><i>Background and Aims</i></b>: There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.</p><p> <b><i>Methods</i></b>: Thirty‐one gallstone patients were enrolled in the study; 17 were treated with 20 mg simvastatin daily for 3 weeks prior to cholecystectomy and 14 served as controls. Samples of blood, liver, gall‐bladder bile and bile from the common bile duct (CBD) were collected and analysed.</p><p> <b><i>Results</i></b>: The plasma cholesterol (−30%), triacylglycerol (−23%) and low‐density lipoprotein (LDL) cholesterol (−42%) concentrations were significantly lowered by simvastatin treatment, as was the plasma lathosterol : cholesterol (−70%), which reflects whole‐body cholesterol synthesis. Despite these changes, the hepatic LDL receptor protein and LDL receptor activity in circulating mononuclear cells were similar in both groups. There were no differences in the plasma phytosterol : cholesterol, which reflects the intestinal cholesterol absorption capacity or in the activity of hepatic acyl‐coenzyme A : cholesterol acyltransferase. There were however, lower cholesterol concentrations in CBD (−68%) and gall bladder (−41%) bile, and decreased lithogenic (−47%) and bile acid hydrophobicity (−22%) indices of CBD bile in the simvastatin group.</p><p> <b><i>Conclusions</i></b>: These data indicate that simvastatin reduced plasma and biliary cholesterol levels primarily by reducing cholesterol synthesis. The reduction in CBD bile lithogenicity and bile acid hydrophobicity by simvastatin suggests that this agent may be useful for people who have early stages of cholesterol gallstone development and in whom a choleretic effect is required.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Simvastatin and gallstone patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of simvastatin on hepatic cholesterol metabolism, bile lithogenicity and bile acid hydrophobicity in patients with gallstones</title></titleInfo><name type="personal"><namePart type="given">Jeffery L</namePart><namePart type="family">Smith</namePart><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul D</namePart><namePart type="family">Roach</namePart><affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Leonie N</namePart><namePart type="family">Wittenberg</namePart><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michel</namePart><namePart type="family">Riottot</namePart><affiliation>Laboratoire de Physiologie de la Nutrition, Université Paris‐Sud, Orsay, France.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. Praga</namePart><namePart type="family">Pillay</namePart><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul J</namePart><namePart type="family">Nestel</namePart><affiliation>CSIRO Division of Health Sciences and Nutrition, Adelaide, South Australia, Australia and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Les K</namePart><namePart type="family">Nathanson</namePart><affiliation>Lipid Metabolism Laboratory, Department of Surgery, The University of Queensland, Royal Brisbane Hospital, Brisbane, Queensland, Australia,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Science Pty</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2000-08</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">6</extent><extent unit="formulas">0</extent><extent unit="references">52</extent><extent unit="linksCrossRef">1</extent><extent unit="words">6383</extent></physicalDescription><abstract>Background and Aims : There is limited information available on the effects of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors on hepatic and biliary cholesterol metabolism in patients with gallstones. The aims of this study were to determine the effect of simvastatin on the regulatory elements of cholesterol metabolism that determine the concentrations of cholesterol in plasma and bile.</abstract><abstract>Methods : Thirty‐one gallstone patients were enrolled in the study; 17 were treated with 20 mg simvastatin daily for 3 weeks prior to cholecystectomy and 14 served as controls. Samples of blood, liver, gall‐bladder bile and bile from the common bile duct (CBD) were collected and analysed.</abstract><abstract>Results : The plasma cholesterol (−30%), triacylglycerol (−23%) and low‐density lipoprotein (LDL) cholesterol (−42%) concentrations were significantly lowered by simvastatin treatment, as was the plasma lathosterol : cholesterol (−70%), which reflects whole‐body cholesterol synthesis. Despite these changes, the hepatic LDL receptor protein and LDL receptor activity in circulating mononuclear cells were similar in both groups. There were no differences in the plasma phytosterol : cholesterol, which reflects the intestinal cholesterol absorption capacity or in the activity of hepatic acyl‐coenzyme A : cholesterol acyltransferase. There were however, lower cholesterol concentrations in CBD (−68%) and gall bladder (−41%) bile, and decreased lithogenic (−47%) and bile acid hydrophobicity (−22%) indices of CBD bile in the simvastatin group.</abstract><abstract>Conclusions : These data indicate that simvastatin reduced plasma and biliary cholesterol levels primarily by reducing cholesterol synthesis. The reduction in CBD bile lithogenicity and bile acid hydrophobicity by simvastatin suggests that this agent may be useful for people who have early stages of cholesterol gallstone development and in whom a choleretic effect is required.</abstract><subject lang="en"><genre>keywords</genre><topic>biliary lipids</topic><topic>choleretic</topic><topic>3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors</topic><topic>low density lipoprotein receptor</topic><topic>lithogenic index</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Gastroenterology and Hepatology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0815-9319</identifier><identifier type="eISSN">1440-1746</identifier><identifier type="DOI">10.1111/(ISSN)1440-1746</identifier><identifier type="PublisherID">JGH</identifier><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>871</start><end>879</end><total>9</total></extent></part></relatedItem><identifier type="istex">3AD559DE21C323983721B84AE422CB10BCD756B8</identifier><identifier type="ark">ark:/67375/WNG-N414FV0X-J</identifier><identifier type="DOI">10.1046/j.1440-1746.2000.02231.x</identifier><identifier type="ArticleID">JGH2231</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Science Pty</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/3AD559DE21C323983721B84AE422CB10BCD756B8/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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