Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?
Identifieur interne : 000701 ( Istex/Corpus ); précédent : 000700; suivant : 000702Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?
Auteurs : Fida Bacha ; Rola Saad ; Neslihan Gungor ; Silva A. ArslanianSource :
- Pediatric Diabetes [ 1399-543X ] ; 2005-06.
English descriptors
- KwdEn :
- Adiponectin, Adiponectin levels, Arslanian, Bacha, Black children, Body composition, Fasting, Fasting adiponectin levels, Higher insulin secretion, Hyperinsulinemia, Insulin, Insulin secretion, Insulin sensitivity, Lower adiponectin levels, Lower insulin sensitivity, Pediatric, Pediatric diabetes, Prepubertal, Prepubertal children, Racial differences, Saad, Similar body composition, White children, White peers.
- Teeft :
- Adiponectin, Adiponectin levels, Arslanian, Bacha, Black children, Body composition, Fasting, Fasting adiponectin levels, Higher insulin secretion, Hyperinsulinemia, Insulin, Insulin secretion, Insulin sensitivity, Lower adiponectin levels, Lower insulin sensitivity, Pediatric, Pediatric diabetes, Prepubertal, Prepubertal children, Racial differences, Saad, Similar body composition, White children, White peers.
Abstract
Abstract: Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p < 0.001). Adiponectin correlated positively with insulin
sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p < 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.
Url:
DOI: 10.1111/j.1399-543X.2005.00108.x
Links to Exploration step
ISTEX:1E2C1015173736ED53DDD33E75765C2BBEEBF21CLe document en format XML
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Arslanian</name><affiliation><mods:affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:1E2C1015173736ED53DDD33E75765C2BBEEBF21C</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1111/j.1399-543X.2005.00108.x</idno><idno type="url">https://api.istex.fr/document/1E2C1015173736ED53DDD33E75765C2BBEEBF21C/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000701</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000701</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?</title><author><name sortKey="Bacha, Fida" sort="Bacha, Fida" uniqKey="Bacha F" first="Fida" last="Bacha">Fida Bacha</name><affiliation><mods:affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: fida.bacha@chp.edu</mods:affiliation></affiliation></author><author><name sortKey="Saad, Rola" sort="Saad, Rola" uniqKey="Saad R" first="Rola" last="Saad">Rola Saad</name><affiliation><mods:affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Gungor, Neslihan" sort="Gungor, Neslihan" uniqKey="Gungor N" first="Neslihan" last="Gungor">Neslihan Gungor</name><affiliation><mods:affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Arslanian, Silva A" sort="Arslanian, Silva A" uniqKey="Arslanian S" first="Silva A." last="Arslanian">Silva A. Arslanian</name><affiliation><mods:affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Pediatric Diabetes</title><title level="j" type="alt">PEDIATRIC DIABETES</title><idno type="ISSN">1399-543X</idno><idno type="eISSN">1399-5448</idno><imprint><biblScope unit="vol">6</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="100">100</biblScope><biblScope unit="page" to="102">102</biblScope><biblScope unit="page-count">3</biblScope><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-06">2005-06</date></imprint><idno type="ISSN">1399-543X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1399-543X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adiponectin</term><term>Adiponectin levels</term><term>Arslanian</term><term>Bacha</term><term>Black children</term><term>Body composition</term><term>Fasting</term><term>Fasting adiponectin levels</term><term>Higher insulin secretion</term><term>Hyperinsulinemia</term><term>Insulin</term><term>Insulin secretion</term><term>Insulin sensitivity</term><term>Lower adiponectin levels</term><term>Lower insulin sensitivity</term><term>Pediatric</term><term>Pediatric diabetes</term><term>Prepubertal</term><term>Prepubertal children</term><term>Racial differences</term><term>Saad</term><term>Similar body composition</term><term>White children</term><term>White peers</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adiponectin</term><term>Adiponectin levels</term><term>Arslanian</term><term>Bacha</term><term>Black children</term><term>Body composition</term><term>Fasting</term><term>Fasting adiponectin levels</term><term>Higher insulin secretion</term><term>Hyperinsulinemia</term><term>Insulin</term><term>Insulin secretion</term><term>Insulin sensitivity</term><term>Lower adiponectin levels</term><term>Lower insulin sensitivity</term><term>Pediatric</term><term>Pediatric diabetes</term><term>Prepubertal</term><term>Prepubertal children</term><term>Racial differences</term><term>Saad</term><term>Similar body composition</term><term>White children</term><term>White peers</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Abstract: Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p < 0.001). Adiponectin correlated positively with insulin
sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p < 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>adiponectin</json:string><json:string>insulin sensitivity</json:string><json:string>black children</json:string><json:string>adiponectin levels</json:string><json:string>hyperinsulinemia</json:string><json:string>insulin</json:string><json:string>lower insulin sensitivity</json:string><json:string>white peers</json:string><json:string>prepubertal</json:string><json:string>lower adiponectin levels</json:string><json:string>fasting</json:string><json:string>pediatric diabetes</json:string><json:string>pediatric</json:string><json:string>bacha</json:string><json:string>white children</json:string><json:string>arslanian</json:string><json:string>saad</json:string><json:string>prepubertal children</json:string><json:string>similar body composition</json:string><json:string>insulin secretion</json:string><json:string>body composition</json:string><json:string>racial differences</json:string><json:string>higher insulin secretion</json:string><json:string>fasting adiponectin levels</json:string></teeft></keywords><author><json:item><name>Fida Bacha</name><affiliations><json:string>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</json:string><json:string>E-mail: fida.bacha@chp.edu</json:string></affiliations></json:item><json:item><name>Rola Saad</name><affiliations><json:string>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item><json:item><name>Neslihan Gungor</name><affiliations><json:string>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item><json:item><name>Silva A. Arslanian</name><affiliations><json:string>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>adiponectin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>African‐American</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>insulin resistance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>insulin secretion</value></json:item></subject><articleId><json:string>PEDI108</json:string></articleId><arkIstex>ark:/67375/WNG-GWMW5L0F-0</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>shortCommunication</json:string></originalGenre><abstract>Abstract: Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p > 0.001). Adiponectin correlated positively with insulin sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p > 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>180</abstractWordCount><abstractCharCount>1368</abstractCharCount><keywordCount>4</keywordCount><score>5.414</score><pdfWordCount>1254</pdfWordCount><pdfCharCount>8248</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>3</pdfPageCount><pdfPageSize>595 x 782 pts</pdfPageSize></qualityIndicators><title>Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?</title><pmid><json:string>15963038</json:string></pmid><genre><json:string>brief-communication</json:string></genre><host><title>Pediatric Diabetes</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1399-5448</json:string></doi><issn><json:string>1399-543X</json:string></issn><eissn><json:string>1399-5448</json:string></eissn><publisherId><json:string>PEDI</json:string></publisherId><volume>6</volume><issue>2</issue><pages><first>100</first><last>102</last><total>3</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2005</json:string></date><geogName></geogName><orgName><json:string>Children’s Hospital of Pittsburgh, Pittsburgh, PA, USA Key</json:string><json:string>Linco Research, St Charles, MO, USA</json:string><json:string>General Clinical Research Center and Eli</json:string><json:string>General Clinical Research Center</json:string><json:string>Division of Endocrinology Children</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Neslihan Gungor</json:string><json:string>Fida Bacha</json:string><json:string>Lynette Orlansky</json:string><json:string>Resa Brna</json:string><json:string>Rola Saad</json:string><json:string>Silva A. 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Division of Endocrinology
Children's Hospital of Pittsburgh
3705 Fifth Avenue, DeSoto Street
Pittsburgh, PA 15213
USA
Tel: +1 412 692 8225;
fax: +1 412 692 5834;
e‐mail: fida.bacha@chp.edu</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Rola</forename><surname>Saad</surname></persName><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Neslihan</forename><surname>Gungor</surname></persName><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Silva A.</forename><surname>Arslanian</surname></persName><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><idno type="istex">1E2C1015173736ED53DDD33E75765C2BBEEBF21C</idno><idno type="ark">ark:/67375/WNG-GWMW5L0F-0</idno><idno type="DOI">10.1111/j.1399-543X.2005.00108.x</idno><idno type="unit">PEDI108</idno><idno type="toTypesetVersion">file:PEDI.PEDI108.pdf</idno></analytic><monogr><title level="j" type="main">Pediatric Diabetes</title><title level="j" type="alt">PEDIATRIC DIABETES</title><idno type="pISSN">1399-543X</idno><idno type="eISSN">1399-5448</idno><idno type="book-DOI">10.1111/(ISSN)1399-5448</idno><idno type="book-part-DOI">10.1111/pdi.2005.6.issue-2</idno><idno type="product">PEDI</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">6</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="100">100</biblScope><biblScope unit="page" to="102">102</biblScope><biblScope unit="page-count">3</biblScope><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-06"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Abstract: </hi> Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p < 0.001). Adiponectin correlated positively with insulin
sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p < 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">adiponectin</term><term xml:id="k2">African‐American</term><term xml:id="k3">insulin resistance</term><term xml:id="k4">insulin secretion </term></keywords><keywords rend="tocHeading1"><term>Brief Report</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/1E2C1015173736ED53DDD33E75765C2BBEEBF21C/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>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK; Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1399-5448</doi><issn type="print">1399-543X</issn><issn type="electronic">1399-5448</issn><idGroup><id type="product" value="PEDI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="PEDIATRIC DIABETES">Pediatric Diabetes</title></titleGroup></publicationMeta><publicationMeta level="part" position="06002"><doi origin="wiley">10.1111/pdi.2005.6.issue-2</doi><numberingGroup><numbering type="journalVolume" number="6">6</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2005-06">June 2005</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="0010000" status="forIssue"><doi origin="wiley">10.1111/j.1399-543X.2005.00108.x</doi><idGroup><id type="unit" value="PEDI108"></id></idGroup><countGroup><count type="pageTotal" number="3"></count></countGroup><titleGroup><title type="tocHeading1">Brief Report</title></titleGroup><eventGroup><event type="firstOnline" date="2005-06-15"></event><event type="publishedOnlineFinalForm" date="2005-06-15"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="100">100</numbering><numbering type="pageLast" number="102">102</numbering></numberingGroup><correspondenceTo>
*Fida Bacha, MD
Division of Endocrinology
Children's Hospital of Pittsburgh
3705 Fifth Avenue, DeSoto Street
Pittsburgh, PA 15213
USA
Tel: +1 412 692 8225;
fax: +1 412 692 5834;
e‐mail: <email>fida.bacha@chp.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PEDI.PEDI108.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Submitted 20 October 2004. Accepted for publication 8 February 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="12"></count><count type="wordTotal" number="986"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?</title><title type="shortAuthors"><b>Bacha et al.</b></title><title type="short"><b>Adiponectin, insulin sensitivity, and secretion in children</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Fida</givenNames><familyName>Bacha</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Rola</givenNames><familyName>Saad</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Neslihan</givenNames><familyName>Gungor</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Silva A.</givenNames><familyName>Arslanian</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">adiponectin</keyword><keyword xml:id="k2">African‐American</keyword><keyword xml:id="k3">insulin resistance</keyword><keyword xml:id="k4">insulin secretion </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!--
Bacha F, Saad R, Gungor N, Arslanian SA. Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African-American children?
--><p><b>Abstract: </b> Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p < 0.001). Adiponectin correlated positively with insulin
sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p < 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Adiponectin, insulin sensitivity, and secretion in children</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Does adiponectin explain the lower insulin sensitivity and hyperinsulinemia of African‐American children?</title></titleInfo><name type="personal"><namePart type="given">Fida</namePart><namePart type="family">Bacha</namePart><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</affiliation><affiliation>E-mail: fida.bacha@chp.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rola</namePart><namePart type="family">Saad</namePart><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Neslihan</namePart><namePart type="family">Gungor</namePart><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Silva A.</namePart><namePart type="family">Arslanian</namePart><affiliation>Division of Endocrinology, Metabolism and Diabetes Mellitus, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="shortCommunication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK; Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2005-06</dateIssued><edition>Submitted 20 October 2004. Accepted for publication 8 February 2005</edition><copyrightDate encoding="w3cdtf">2005</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">0</extent><extent unit="formulas">0</extent><extent unit="references">12</extent><extent unit="linksCrossRef">0</extent><extent unit="words">986</extent></physicalDescription><abstract>Abstract: Adiponectin is an adipocytokine with antidiabetogenic properties. The present study investigated: (i) the effect of race on adiponectin levels and (ii) the relationship of adiponectin levels in children to insulin sensitivity and secretion. Fasting adiponectin levels were determined in 22 healthy prepubertal black compared with 22 white children of similar body composition. We previously reported these black children to have lower insulin sensitivity and higher first‐phase insulin secretion than their white peers. Fasting adiponectin levels were lower in black children (9.9 ± 1.0 µg/mL vs. 15.7 ± 1.1 µg/mL, p < 0.001). Adiponectin correlated positively with insulin
sensitivity (r = 0.29, p = 0.06) and negatively with first‐phase insulin levels (r = −0.47, p = 0.001). In a multiple regression analysis, 48% of the variance in first‐phase insulin secretion was explained by the independent effects of race (p = 0.017), adiponectin (p = 0.03), and percentage of body fat (p < 0.001). Adiponectin did not contribute significantly to the variance in insulin sensitivity. In summary, black children have approximately 35% lower adiponectin levels than their white peers. Lower adiponectin does not seem to explain the racial differences in insulin sensitivity. The relationship of hyperinsulinemia and hypoadiponectinemia needs to be further explored.</abstract><subject lang="en"><genre>keywords</genre><topic>adiponectin</topic><topic>African‐American</topic><topic>insulin resistance</topic><topic>insulin secretion</topic></subject><relatedItem type="host"><titleInfo><title>Pediatric Diabetes</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">1399-543X</identifier><identifier type="eISSN">1399-5448</identifier><identifier type="DOI">10.1111/(ISSN)1399-5448</identifier><identifier type="PublisherID">PEDI</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>100</start><end>102</end><total>3</total></extent></part></relatedItem><identifier type="istex">1E2C1015173736ED53DDD33E75765C2BBEEBF21C</identifier><identifier type="ark">ark:/67375/WNG-GWMW5L0F-0</identifier><identifier type="DOI">10.1111/j.1399-543X.2005.00108.x</identifier><identifier type="ArticleID">PEDI108</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>Munksgaard International Publishers</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/1E2C1015173736ED53DDD33E75765C2BBEEBF21C/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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