Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system
Identifieur interne : 001071 ( Istex/Corpus ); précédent : 001070; suivant : 001072Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system
Auteurs : Maria Teresa Pellecchia ; Rosario Pivonello ; Katia Longo ; Michela Manfredi ; Alessandro Tessitore ; Marianna Amboni ; Claudia Pivonello ; Mariangela Rocco ; Autilia Cozzolino ; Annamaria Colao ; Paolo BaroneSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
English descriptors
Abstract
Insulin‐like growth factors (IGF‐I and IGF‐II) have been shown to have several neurotrophic actions and IGF system may be impaired in neurodegenerative disorders. The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of IGF‐I, IGF‐II, insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; p = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, p = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score <26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, p = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.
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DOI: 10.1002/mds.23320
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last="Tessitore">Alessandro Tessitore</name><affiliation><mods:affiliation>Department of Neurological Sciences, Second University of Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Amboni, Marianna" sort="Amboni, Marianna" uniqKey="Amboni M" first="Marianna" last="Amboni">Marianna Amboni</name><affiliation><mods:affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Pivonello, Claudia" sort="Pivonello, Claudia" uniqKey="Pivonello C" first="Claudia" last="Pivonello">Claudia Pivonello</name><affiliation><mods:affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Rocco, Mariangela" sort="Rocco, Mariangela" uniqKey="Rocco M" first="Mariangela" last="Rocco">Mariangela Rocco</name><affiliation><mods:affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Cozzolino, Autilia" sort="Cozzolino, Autilia" uniqKey="Cozzolino A" first="Autilia" last="Cozzolino">Autilia Cozzolino</name><affiliation><mods:affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Colao, Annamaria" sort="Colao, Annamaria" uniqKey="Colao A" first="Annamaria" last="Colao">Annamaria Colao</name><affiliation><mods:affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</mods:affiliation></affiliation></author><author><name sortKey="Barone, Paolo" sort="Barone, Paolo" uniqKey="Barone P" first="Paolo" last="Barone">Paolo Barone</name><affiliation><mods:affiliation>Department of Neurological Sciences, 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15">2010-11-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2621">2621</biblScope><biblScope unit="page" to="2626">2626</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9ED7A201D394460BFF602344192903ED8D9B5992</idno><idno type="DOI">10.1002/mds.23320</idno><idno type="ArticleID">MDS23320</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>insulin</term><term>insulin‐like growth factors</term><term>multiple system atrophy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Insulin‐like growth factors (IGF‐I and IGF‐II) have been shown to have several neurotrophic actions and IGF system may be impaired in neurodegenerative disorders. The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of IGF‐I, IGF‐II, insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; p = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, p = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score <26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, p = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Maria Teresa Pellecchia</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Rosario Pivonello</name><affiliations><json:string>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Katia Longo</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string><json:string>IDC Hermitage‐Capodimonte, Naples, Italy</json:string></affiliations></json:item><json:item><name>Michela Manfredi</name><affiliations><json:string>Department of Neurorehabilitation, Salvatore Maugeri IRCCS, Castel Goffredo, Italy</json:string></affiliations></json:item><json:item><name>Alessandro Tessitore</name><affiliations><json:string>Department of Neurological Sciences, Second University of Naples, Italy</json:string></affiliations></json:item><json:item><name>Marianna Amboni</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string><json:string>IDC Hermitage‐Capodimonte, Naples, Italy</json:string></affiliations></json:item><json:item><name>Claudia Pivonello</name><affiliations><json:string>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Mariangela Rocco</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Autilia Cozzolino</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Annamaria Colao</name><affiliations><json:string>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</json:string></affiliations></json:item><json:item><name>Paolo Barone</name><affiliations><json:string>Department of Neurological Sciences, Federico II University, Naples, Italy</json:string><json:string>IDC Hermitage‐Capodimonte, Naples, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>insulin‐like growth factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>insulin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>multiple system atrophy</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Insulin‐like growth factors (IGF‐I and IGF‐II) have been shown to have several neurotrophic actions and IGF system may be impaired in neurodegenerative disorders. The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of IGF‐I, IGF‐II, insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; p = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, p = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score >26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, p = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.</abstract><qualityIndicators><score>6.571</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1533</abstractCharCount><pdfWordCount>3571</pdfWordCount><pdfCharCount>23192</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>250</abstractWordCount></qualityIndicators><title>Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system</title><genre><json:string>Serial article</json:string></genre><host><volume>25</volume><pages><total>6</total><last>2626</last><first>2621</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</issue><subject><json:item><value>Research 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xml:lang="en">Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system</title><author><persName><forename type="first">Maria Teresa</forename><surname>Pellecchia</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Rosario</forename><surname>Pivonello</surname></persName><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Katia</forename><surname>Longo</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation></author><author><persName><forename type="first">Michela</forename><surname>Manfredi</surname></persName><affiliation>Department of Neurorehabilitation, Salvatore Maugeri IRCCS, Castel Goffredo, Italy</affiliation></author><author><persName><forename type="first">Alessandro</forename><surname>Tessitore</surname></persName><affiliation>Department of Neurological Sciences, Second University of Naples, Italy</affiliation></author><author><persName><forename type="first">Marianna</forename><surname>Amboni</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation></author><author><persName><forename type="first">Claudia</forename><surname>Pivonello</surname></persName><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Mariangela</forename><surname>Rocco</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Autilia</forename><surname>Cozzolino</surname></persName><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Annamaria</forename><surname>Colao</surname></persName><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation></author><author><persName><forename type="first">Paolo</forename><surname>Barone</surname></persName><note type="correspondence"><p>Correspondence: Department of Neurological Sciences, University “Federico II”–IDC Hermitage Capodimonte, Via S. Pansini 5, 80131 Naples, Italy</p></note><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of IGF‐I, IGF‐II, insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; p = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, p = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score <26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, p = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>insulin‐like growth factors</term></item><item><term>insulin</term></item><item><term>multiple system atrophy</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-01-02">Received</change><change when="2010-05-27">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9ED7A201D394460BFF602344192903ED8D9B5992/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="150"><doi origin="wiley" registered="yes">10.1002/mds.v25:15</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">15</numbering></numberingGroup><coverDate startDate="2010-11-15">15 November 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="200" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23320</doi><idGroup><id type="unit" value="MDS23320"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-01-02"></event><event type="manuscriptRevised" date="2010-01-29"></event><event type="manuscriptAccepted" date="2010-05-27"></event><event type="firstOnline" date="2010-08-03"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-08-03"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.9 mode:FullText" date="2013-01-24"></event><event type="publishedOnlineFinalForm" date="2010-11-10"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">2621</numbering><numbering type="pageLast">2626</numbering></numberingGroup><correspondenceTo>Department of Neurological Sciences, University “Federico II”–IDC Hermitage Capodimonte, Via S. Pansini 5, 80131 Naples, Italy</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23320.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="4579"></count></countGroup><titleGroup><title type="main" xml:lang="en">Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system<link href="#fn1"></link></title><title type="short" xml:lang="en">Insulin‐Like Growth Factors In MSA</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Maria Teresa</givenNames><familyName>Pellecchia</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Rosario</givenNames><familyName>Pivonello</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Katia</givenNames><familyName>Longo</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Michela</givenNames><familyName>Manfredi</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Alessandro</givenNames><familyName>Tessitore</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Marianna</givenNames><familyName>Amboni</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Claudia</givenNames><familyName>Pivonello</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mariangela</givenNames><familyName>Rocco</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Autilia</givenNames><familyName>Cozzolino</familyName></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Annamaria</givenNames><familyName>Colao</familyName></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1 #af3" corresponding="yes"><personName><givenNames>Paolo</givenNames><familyName>Barone</familyName></personName><contactDetails><email>barone@unina.it</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IT" type="organization"><unparsedAffiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="IT" type="organization"><unparsedAffiliation>IDC Hermitage‐Capodimonte, Naples, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurorehabilitation, Salvatore Maugeri IRCCS, Castel Goffredo, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological Sciences, Second University of Naples, Italy</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">insulin‐like growth factors</keyword><keyword xml:id="kwd2">insulin</keyword><keyword xml:id="kwd3">multiple system atrophy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Insulin‐like growth factors (IGF‐I and IGF‐II) have been shown to have several neurotrophic actions and IGF system may be impaired in neurodegenerative disorders. The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of <sc>IGF‐I, IGF‐II,</sc> insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; <i>p</i> = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, <i>p</i> = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score <26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, <i>p</i> = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Insulin‐Like Growth Factors In MSA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Multiple system atrophy is associated with changes in peripheral insulin‐like growth factor system</title></titleInfo><name type="personal"><namePart type="given">Maria Teresa</namePart><namePart type="family">Pellecchia</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rosario</namePart><namePart type="family">Pivonello</namePart><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katia</namePart><namePart type="family">Longo</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michela</namePart><namePart type="family">Manfredi</namePart><affiliation>Department of Neurorehabilitation, Salvatore Maugeri IRCCS, Castel Goffredo, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alessandro</namePart><namePart type="family">Tessitore</namePart><affiliation>Department of Neurological Sciences, Second University of Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marianna</namePart><namePart type="family">Amboni</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Pivonello</namePart><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mariangela</namePart><namePart type="family">Rocco</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Autilia</namePart><namePart type="family">Cozzolino</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Annamaria</namePart><namePart type="family">Colao</namePart><affiliation>Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paolo</namePart><namePart type="family">Barone</namePart><affiliation>Department of Neurological Sciences, Federico II University, Naples, Italy</affiliation><affiliation>IDC Hermitage‐Capodimonte, Naples, Italy</affiliation><description>Correspondence: Department of Neurological Sciences, University “Federico II”–IDC Hermitage Capodimonte, Via S. Pansini 5, 80131 Naples, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-01-02</dateCaptured><dateValid encoding="w3cdtf">2010-05-27</dateValid><copyrightDate encoding="w3cdtf">2010</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="figures">3</extent><extent unit="tables">2</extent><extent unit="references">38</extent><extent unit="words">4579</extent></physicalDescription><abstract lang="en">Insulin‐like growth factors (IGF‐I and IGF‐II) have been shown to have several neurotrophic actions and IGF system may be impaired in neurodegenerative disorders. The aim of this study was to investigate the IGF system in patients with MSA and to evaluate correlations between this endocrine system and clinical features of the disease. Serum levels of IGF‐I, IGF‐II, insulin, IGF‐binding protein 1 (BP1), and IGF‐binding protein 3 (BP3) were measured in 25 patients with probable MSA and 25 age, sex and BMI‐matched healthy controls. Clinical status of each patient was evaluated with the Unified Multiple System Atrophy Rating Scale (UMSARS) Part II and the Hoehn and Yahr rating scale. IGF‐I levels were significantly higher in MSA (164.1 + 66.2 μg/L) than in healthy controls (111.7 + 60.3 μg/L; p = 0.001). Insulin levels were significantly higher in MSA patients (21.9 ± 14.4 μU/mL) than in healthy controls (13.3 ± 5.1 μU/mL, p = 0.048). No significant difference was found in serum IGF‐II, IGF‐BP1, and IGF‐ BP3 levels between patients with MSA and healthy controls. There was a trend toward significantly higher IGF‐II levels in MSA patients with UMSARS score <26 (1026.3 ± 442.6 μg/L) than MSA patients with UMSARS score >26 (796.1 ± 234 μg/L, p = 0.055). The results of this study demonstrated that IGF system is altered in MSA. The degenerative process in MSA could lead to a compensatory increase in IGF‐I and insulin in an attempt to provide additional support to degenerating neurons. © 2010 Movement Disorder Society.</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><subject lang="en"><genre>Keywords</genre><topic>insulin‐like growth factors</topic><topic>insulin</topic><topic>multiple system atrophy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2621</start><end>2626</end><total>6</total></extent></part></relatedItem><identifier type="istex">9ED7A201D394460BFF602344192903ED8D9B5992</identifier><identifier type="DOI">10.1002/mds.23320</identifier><identifier type="ArticleID">MDS23320</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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