The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins
Identifieur interne : 000D52 ( Istex/Corpus ); précédent : 000D51; suivant : 000D53The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins
Auteurs : R. P. F. Dullaart ; K. Hoogenberg ; J. E. M. Groener ; L. D. Dikkescheo ; D. W. Erkelens ; H. DoorenbosSource :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 1990-12.
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Abstract
Abstract. The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P < 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (P < 0.02), free cholesterol (P < 0.001), triacylglycerol (P < 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (P < 0.01) were inversely related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.
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DOI: 10.1111/j.1365-2362.1990.tb01904.x
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Groener</name><affiliation><mods:affiliation>*Department of Biochemistry I, Erasmus University Rotterdam</mods:affiliation></affiliation></author><author><name sortKey="Dikkescheo, L D" sort="Dikkescheo, L D" uniqKey="Dikkescheo L" first="L. D." last="Dikkescheo">L. D. Dikkescheo</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</mods:affiliation></affiliation></author><author><name sortKey="Erkelens, D W" sort="Erkelens, D W" uniqKey="Erkelens D" first="D. W." last="Erkelens">D. W. Erkelens</name><affiliation><mods:affiliation>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Doorenbos, H" sort="Doorenbos, H" uniqKey="Doorenbos H" first="H." last="Doorenbos">H. Doorenbos</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1111/j.1365-2362.1990.tb01904.x</idno><idno type="url">https://api.istex.fr/document/0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000D52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title><author><name sortKey="Dullaart, R P F" sort="Dullaart, R P F" uniqKey="Dullaart R" first="R. P. F." last="Dullaart">R. P. F. Dullaart</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</mods:affiliation></affiliation></author><author><name sortKey="Hoogenberg, K" sort="Hoogenberg, K" uniqKey="Hoogenberg K" first="K." last="Hoogenberg">K. Hoogenberg</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</mods:affiliation></affiliation></author><author><name sortKey="Groener, J E M" sort="Groener, J E M" uniqKey="Groener J" first="J. E. M." last="Groener">J. E. M. Groener</name><affiliation><mods:affiliation>*Department of Biochemistry I, Erasmus University Rotterdam</mods:affiliation></affiliation></author><author><name sortKey="Dikkescheo, L D" sort="Dikkescheo, L D" uniqKey="Dikkescheo L" first="L. D." last="Dikkescheo">L. D. Dikkescheo</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</mods:affiliation></affiliation></author><author><name sortKey="Erkelens, D W" sort="Erkelens, D W" uniqKey="Erkelens D" first="D. W." last="Erkelens">D. W. Erkelens</name><affiliation><mods:affiliation>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Doorenbos, H" sort="Doorenbos, H" uniqKey="Doorenbos H" first="H." last="Doorenbos">H. Doorenbos</name><affiliation><mods:affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</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="1990-12">1990-12</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="581">581</biblScope><biblScope unit="page" to="587">587</biblScope></imprint><idno type="ISSN">0014-2972</idno></series><idno type="istex">0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E</idno><idno type="DOI">10.1111/j.1365-2362.1990.tb01904.x</idno><idno type="ArticleID">ECI581</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cholesterol metabolism</term><term>cholesteryl ester transfer activity</term><term>high‐density lipoproteins</term><term>hypothyroidism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract. The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P < 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (P < 0.02), free cholesterol (P < 0.001), triacylglycerol (P < 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (P < 0.01) were inversely related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>R. P. F. DULLAART</name><affiliations><json:string>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</json:string></affiliations></json:item><json:item><name>K. HOOGENBERG</name><affiliations><json:string>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</json:string></affiliations></json:item><json:item><name>J. E. M. GROENER</name><affiliations><json:string>*Department of Biochemistry I, Erasmus University Rotterdam</json:string></affiliations></json:item><json:item><name>L. D. DIKKESCHEO</name><affiliations><json:string>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</json:string></affiliations></json:item><json:item><name>D. W. ERKELENS</name><affiliations><json:string>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</json:string></affiliations></json:item><json:item><name>H. DOORENBOS</name><affiliations><json:string>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Cholesterol metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cholesteryl ester transfer activity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>high‐density lipoproteins</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypothyroidism</value></json:item></subject><articleId><json:string>ECI581</json:string></articleId><language><json:string>eng</json:string></language><abstract>Abstract. The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P > 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (P > 0.02), free cholesterol (P > 0.001), triacylglycerol (P > 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (P > 0.01) were inversely related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.</abstract><qualityIndicators><score>7.09</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1587</abstractCharCount><pdfWordCount>4510</pdfWordCount><pdfCharCount>28378</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>215</abstractWordCount></qualityIndicators><title>The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title><genre><json:string>article</json:string></genre><host><volume>20</volume><publisherId><json:string>ECI</json:string></publisherId><pages><total>7</total><last>587</last><first>581</first></pages><issn><json:string>0014-2972</json:string></issn><issue>6</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>1990</publicationDate><copyrightDate>1990</copyrightDate><doi><json:string>10.1111/j.1365-2362.1990.tb01904.x</json:string></doi><id>0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1990</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title><author><persName><forename type="first">R. P. F.</forename><surname>DULLAART</surname></persName><note type="correspondence"><p>Correspondence: Department of Endocrinology. University Hospital. Oostersingel 59, 9713 FZ Groningen, The Netherlands.</p></note><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation></author><author><persName><forename type="first">K.</forename><surname>HOOGENBERG</surname></persName><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation></author><author><persName><forename type="first">J. E. M.</forename><surname>GROENER</surname></persName><affiliation>*Department of Biochemistry I, Erasmus University Rotterdam</affiliation></author><author><persName><forename type="first">L. D.</forename><surname>DIKKESCHEO</surname></persName><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation></author><author><persName><forename type="first">D. W.</forename><surname>ERKELENS</surname></persName><affiliation>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</affiliation></author><author><persName><forename type="first">H.</forename><surname>DOORENBOS</surname></persName><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</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="1990-12"></date><biblScope unit="volume">20</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="581">581</biblScope><biblScope unit="page" to="587">587</biblScope></imprint></monogr><idno type="istex">0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E</idno><idno type="DOI">10.1111/j.1365-2362.1990.tb01904.x</idno><idno type="ArticleID">ECI581</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1990</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract. The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P < 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (P < 0.02), free cholesterol (P < 0.001), triacylglycerol (P < 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (P < 0.01) were inversely related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Cholesterol metabolism</term></item><item><term>cholesteryl ester transfer activity</term></item><item><term>high‐density lipoproteins</term></item><item><term>hypothyroidism</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1990-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E/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="12006"><doi origin="wiley">10.1111/eci.1990.20.issue-6</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="1990-12">December 1990</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0058100" status="forIssue"><doi origin="wiley">10.1111/j.1365-2362.1990.tb01904.x</doi><idGroup><id type="unit" value="ECI581"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><eventGroup><event type="firstOnline" date="2008-06-28"></event><event type="publishedOnlineFinalForm" date="2008-06-28"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText" date="2010-07-23"></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="581">581</numbering><numbering type="pageLast" number="587">587</numbering></numberingGroup><correspondenceTo>Department of Endocrinology. University Hospital. Oostersingel 59, 9713 FZ Groningen, The Netherlands.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ECI.ECI581.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 26 September 1989 and in revised form 20 April 1990</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="61"></count><count type="linksCrossRef" number="7"></count></countGroup><titleGroup><title type="main">The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>R. P. F.</givenNames><familyName>DULLAART</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>K.</givenNames><familyName>HOOGENBERG</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>J. E. M.</givenNames><familyName>GROENER</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>L. D.</givenNames><familyName>DIKKESCHEO</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>D. W.</givenNames><familyName>ERKELENS</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>H.</givenNames><familyName>DOORENBOS</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>*Department of Biochemistry I, Erasmus University Rotterdam</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="NL"><unparsedAffiliation>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Cholesterol metabolism</keyword><keyword xml:id="k2">cholesteryl ester transfer activity</keyword><keyword xml:id="k3">high‐density lipoproteins</keyword><keyword xml:id="k4">hypothyroidism</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Abstract. </b> The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days.</p><p>During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A<sub>1</sub> and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (<i>P</i> < 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (<i>P</i> < 0.02), free cholesterol (<i>P</i> < 0.001), triacylglycerol (<i>P</i> < 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (<i>P</i> < 0.01) were inversely related to the changes in cholesteryl ester transfer activity.</p><p>We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high‐density lipoproteins</title></titleInfo><name type="personal"><namePart type="given">R. P. F.</namePart><namePart type="family">DULLAART</namePart><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation><description>Correspondence: Department of Endocrinology. University Hospital. Oostersingel 59, 9713 FZ Groningen, The Netherlands.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">HOOGENBERG</namePart><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. E. M.</namePart><namePart type="family">GROENER</namePart><affiliation>*Department of Biochemistry I, Erasmus University Rotterdam</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L. D.</namePart><namePart type="family">DIKKESCHEO</namePart><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. W.</namePart><namePart type="family">ERKELENS</namePart><affiliation>†Department of Internal Medicine, University Hospital Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">DOORENBOS</namePart><affiliation>Departments of Endocrinology and Clinical Chemistry, University Hospital Groningen</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1990-12</dateIssued><edition>Received 26 September 1989 and in revised form 20 April 1990</edition><copyrightDate encoding="w3cdtf">1990</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">61</extent></physicalDescription><abstract lang="en">Abstract. The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low‐density and high‐density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very‐low‐ plus low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P < 0.02), and an effect of treatment duration was observed. The changes in high‐density lipoprotein total cholesterol (P < 0.02), free cholesterol (P < 0.001), triacylglycerol (P < 0.05) and the free cholesterol/cholesteryl ester molar ratio in high‐density lipoproteins (P < 0.01) were inversely related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high‐density lipoprotein lipids observed in hypothyroidism.</abstract><subject lang="en"><genre>Keywords</genre><topic>Cholesterol metabolism</topic><topic>cholesteryl ester transfer activity</topic><topic>high‐density lipoproteins</topic><topic>hypothyroidism</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>1990</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>581</start><end>587</end><total>7</total></extent></part></relatedItem><identifier type="istex">0EC32DB1E4C0F3EEF7D13383349A4B5B96A8757E</identifier><identifier type="DOI">10.1111/j.1365-2362.1990.tb01904.x</identifier><identifier type="ArticleID">ECI581</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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