Impaired insulin sensitivity and secretion in normoglycemic patients with spinocerebellar ataxia type 1
Identifieur interne : 000378 ( Istex/Corpus ); précédent : 000377; suivant : 000379Impaired insulin sensitivity and secretion in normoglycemic patients with spinocerebellar ataxia type 1
Auteurs : Nebojša M. Lali ; Nataša Dragaševi ; Elka Stefanova ; Aleksandra Joti ; Katarina Lali ; Tanja Mili I ; Igor Petrovi ; Marija Ma Eši ; Vladimir S. KostiSource :
- Movement Disorders [ 0885-3185 ] ; 2010-09-15.
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Abstract
We have recently shown an impairment in insulin sensitivity and insulin secretion in normoglycemic patients with Huntington disease (HD). To investigate whether such observations are HD‐specific or may be common to other polyglutamine diseases, glucose homeostasis was studied in 12 unrelated, untreated normoglycemic patients with spinocerebellar ataxia type 1 (SCA1), another entity from the family of polyglutamine diseases, and 24 healthy, matched controls. Metabolic investigations included (a) glucose tolerance assessment on the basis of glucose curve during oral glucose challenge; (b) insulin sensitivity assessment by the homeostasis model assessment (HOMA) and the euglycemic insulin clamp (M value); and (c) insulin secretion by acute insulin response (AIR) and insulinogenic index. The evaluation of insulin sensitivity demonstrated higher HOMA‐insulin resistance indices, and lower M values (P < 0.001 and P < 0.05, respectively), while both the AIR and the insulinogenic index were lower in patients with SCA1 compared to controls (P < 0.001 and P < 0.05, respectively). Our data suggested an impairment in insulin secretion capacity, as well as simultaneous decrease in insulin sensitivity, with an increase in insulin resistance level in patients with SCA1. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23176
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ISTEX:1CB91F429E3A4A34BAE56F764EEC759C4AFB0DC1Le document en format XML
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Dr Subotića 6, Belgrade 11000, Serbia</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23176.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="13"></count><count type="wordTotal" number="2926"></count></countGroup><titleGroup><title type="main" xml:lang="en">Impaired insulin sensitivity and secretion in normoglycemic patients with spinocerebellar ataxia type 1<link href="#fn3"></link></title><title type="short" xml:lang="en">Insulin Sensitivity and Secretion in SCA1</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Nebojša M.</givenNames><familyName>Lalić</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>NatašA</givenNames><familyName>Dragašević</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Elka</givenNames><familyName>Stefanova</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Aleksandra</givenNames><familyName>Jotić</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Katarina</givenNames><familyName>Lalić</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tanja</givenNames><familyName>Miličić</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Igor</givenNames><familyName>Petrović</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marija</givenNames><familyName>Maćešić</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><givenNames>Vladimir S.</givenNames><familyName>Kostić</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>vladimir.s.kostic@gmail.com</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="RS" type="organization"><unparsedAffiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="RS" type="organization"><unparsedAffiliation>Clinical Center of Serbia, Institute of Neurology, Belgrade, Serbia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">spinocerebellar ataxia</keyword><keyword xml:id="kwd2">insulin resistance</keyword></keywordGroup><fundingInfo><fundingAgency>Ministry of Science, Republic of Serbia</fundingAgency><fundingNumber>projects no. 145057</fundingNumber><fundingNumber>145089</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We have recently shown an impairment in insulin sensitivity and insulin secretion in normoglycemic patients with Huntington disease (HD). To investigate whether such observations are HD‐specific or may be common to other polyglutamine diseases, glucose homeostasis was studied in 12 unrelated, untreated normoglycemic patients with spinocerebellar ataxia type 1 (SCA1), another entity from the family of polyglutamine diseases, and 24 healthy, matched controls. Metabolic investigations included (a) glucose tolerance assessment on the basis of glucose curve during oral glucose challenge; (b) insulin sensitivity assessment by the homeostasis model assessment (HOMA) and the euglycemic insulin clamp (<i>M</i> value); and (c) insulin secretion by acute insulin response (AIR) and insulinogenic index. The evaluation of insulin sensitivity demonstrated higher HOMA‐insulin resistance indices, and lower <i>M</i> values (<i>P</i> < 0.001 and <i>P</i> < 0.05, respectively), while both the AIR and the insulinogenic index were lower in patients with SCA1 compared to controls (<i>P</i> < 0.001 and <i>P</i> < 0.05, respectively). Our data suggested an impairment in insulin secretion capacity, as well as simultaneous decrease in insulin sensitivity, with an increase in insulin resistance level in patients with SCA1. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p>State on ghost‐writing: There is no ghost‐writing by any one not named on the author list</p><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impaired insulin sensitivity and secretion in normoglycemic patients with spinocerebellar ataxia type 1</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Insulin Sensitivity and Secretion in SCA1</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impaired insulin sensitivity and secretion in normoglycemic patients with spinocerebellar ataxia type 1</title></titleInfo><name type="personal"><namePart type="given">Nebojša M.</namePart><namePart type="family">Lalić</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NatašA</namePart><namePart type="family">Dragašević</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute of Neurology, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elka</namePart><namePart type="family">Stefanova</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute of Neurology, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aleksandra</namePart><namePart type="family">Jotić</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katarina</namePart><namePart type="family">Lalić</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tanja</namePart><namePart type="family">Miličić</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Igor</namePart><namePart type="family">Petrović</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinical Center of Serbia, Institute of Neurology, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marija</namePart><namePart type="family">Maćešić</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vladimir S.</namePart><namePart type="family">Kostić</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Center of Serbia, Institute of Neurology, Belgrade, Serbia</affiliation><affiliation>Institute of Neurology CCS, Ul. Dr Subotića 6, Belgrade 11000, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-09-15</dateIssued><dateCaptured encoding="w3cdtf">2009-12-04</dateCaptured><dateValid encoding="w3cdtf">2010-03-22</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">1</extent><extent unit="tables">1</extent><extent unit="references">13</extent><extent unit="words">2926</extent></physicalDescription><abstract lang="en">We have recently shown an impairment in insulin sensitivity and insulin secretion in normoglycemic patients with Huntington disease (HD). To investigate whether such observations are HD‐specific or may be common to other polyglutamine diseases, glucose homeostasis was studied in 12 unrelated, untreated normoglycemic patients with spinocerebellar ataxia type 1 (SCA1), another entity from the family of polyglutamine diseases, and 24 healthy, matched controls. Metabolic investigations included (a) glucose tolerance assessment on the basis of glucose curve during oral glucose challenge; (b) insulin sensitivity assessment by the homeostasis model assessment (HOMA) and the euglycemic insulin clamp (M value); and (c) insulin secretion by acute insulin response (AIR) and insulinogenic index. The evaluation of insulin sensitivity demonstrated higher HOMA‐insulin resistance indices, and lower M values (P < 0.001 and P < 0.05, respectively), while both the AIR and the insulinogenic index were lower in patients with SCA1 compared to controls (P < 0.001 and P < 0.05, respectively). Our data suggested an impairment in insulin secretion capacity, as well as simultaneous decrease in insulin sensitivity, with an increase in insulin resistance level in patients with SCA1. © 2010 Movement Disorder Society</abstract><note type="content">*State on ghost‐writing: There is no ghost‐writing by any one not named on the author list Potential conflict of interest: Nothing to report.</note><note type="funding">Ministry of Science, Republic of Serbia - No. projects no. 145057; No. 145089; </note><subject lang="en"><genre>keywords</genre><topic>spinocerebellar ataxia</topic><topic>insulin resistance</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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