Movement Disorders (revue)

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Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1

Identifieur interne : 000914 ( PascalFrancis/Corpus ); précédent : 000913; suivant : 000915

Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1

Auteurs : Nebojša M. Lalic ; Nataša Dragasevic ; Elka Stefanova ; Aleksandra Jotic ; Katarina Lalic ; Tanja Milicic ; Igor Petrovic ; Marija Macesic ; Vladimir S. Kostic

Source :

RBID : Pascal:10-0446317

Descripteurs français

English descriptors

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0885-3185
A03   1    @0 Mov. disord.
A05       @2 25
A06       @2 12
A08 01  1  ENG  @1 Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1
A11 01  1    @1 LALIC (Nebojša M.)
A11 02  1    @1 DRAGASEVIC (Nataša)
A11 03  1    @1 STEFANOVA (Elka)
A11 04  1    @1 JOTIC (Aleksandra)
A11 05  1    @1 LALIC (Katarina)
A11 06  1    @1 MILICIC (Tanja)
A11 07  1    @1 PETROVIC (Igor)
A11 08  1    @1 MACESIC (Marija)
A11 09  1    @1 KOSTIC (Vladimir S.)
A14 01      @1 Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases @2 Belgrade @3 SRB @Z 1 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 8 aut.
A14 02      @1 Clinical Center of Serbia, Institute of Neurology @2 Belgrade @3 SRB @Z 2 aut. @Z 3 aut. @Z 7 aut. @Z 9 aut.
A20       @1 1976-1980
A21       @1 2010
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000194841700290
A44       @0 0000 @1 © 2010 INIST-CNRS. All rights reserved.
A45       @0 13 ref.
A47 01  1    @0 10-0446317
A60       @1 P @3 CC
A61       @0 A
A64 01  1    @0 Movement disorders
A66 01      @0 USA
C01 01    ENG  @0 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.
C02 01  X    @0 002B17
C02 02  X    @0 002B17F
C03 01  X  FRE  @0 Insulinorésistance @2 NM @5 01
C03 01  X  ENG  @0 Insulin resistance @2 NM @5 01
C03 01  X  SPA  @0 Resistancia insulina @2 NM @5 01
C03 02  X  FRE  @0 Pathologie du système nerveux @5 02
C03 02  X  ENG  @0 Nervous system diseases @5 02
C03 02  X  SPA  @0 Sistema nervioso patología @5 02
C03 03  X  FRE  @0 Insuline @5 09
C03 03  X  ENG  @0 Insulin @5 09
C03 03  X  SPA  @0 Insulina @5 09
C03 04  X  FRE  @0 Sensibilité @5 10
C03 04  X  ENG  @0 Sensitivity @5 10
C03 04  X  SPA  @0 Sensibilidad @5 10
C03 05  X  FRE  @0 Homme @5 11
C03 05  X  ENG  @0 Human @5 11
C03 05  X  SPA  @0 Hombre @5 11
C03 06  X  FRE  @0 Ataxie spinocérébelleuse @2 NM @5 12
C03 06  X  ENG  @0 Spinocerebellar ataxia @2 NM @5 12
C03 06  X  SPA  @0 Ataxia spinocerebelosa @2 NM @5 12
C07 01  X  FRE  @0 Hormone pancréatique @5 37
C07 01  X  ENG  @0 Pancreatic hormone @5 37
C07 01  X  SPA  @0 Hormona pancreática @5 37
C07 02  X  FRE  @0 Maladie dégénérative @5 38
C07 02  X  ENG  @0 Degenerative disease @5 38
C07 02  X  SPA  @0 Enfermedad degenerativa @5 38
C07 03  X  FRE  @0 Maladie héréditaire @5 39
C07 03  X  ENG  @0 Genetic disease @5 39
C07 03  X  SPA  @0 Enfermedad hereditaria @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
C07 05  X  FRE  @0 Endocrinopathie @5 42
C07 05  X  ENG  @0 Endocrinopathy @5 42
C07 05  X  SPA  @0 Endocrinopatía @5 42
C07 06  X  FRE  @0 Maladie métabolique @5 43
C07 06  X  ENG  @0 Metabolic diseases @5 43
C07 06  X  SPA  @0 Metabolismo patología @5 43
C07 07  X  FRE  @0 Résistance tissu cible @5 44
C07 07  X  ENG  @0 Target tissue resistance @5 44
C07 07  X  SPA  @0 Resistencia tejido blanco @5 44
N21       @1 291
N44 01      @1 OTO
N82       @1 OTO

Format Inist (serveur)

NO : PASCAL 10-0446317 INIST
ET : Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1
AU : LALIC (Nebojša M.); DRAGASEVIC (Nataša); STEFANOVA (Elka); JOTIC (Aleksandra); LALIC (Katarina); MILICIC (Tanja); PETROVIC (Igor); MACESIC (Marija); KOSTIC (Vladimir S.)
AF : Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases/Belgrade/Serbie (1 aut., 4 aut., 5 aut., 6 aut., 8 aut.); Clinical Center of Serbia, Institute of Neurology/Belgrade/Serbie (2 aut., 3 aut., 7 aut., 9 aut.)
DT : Publication en série; Courte communication, note brève; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 12; Pp. 1976-1980; Bibl. 13 ref.
LA : Anglais
EA : 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.
CC : 002B17; 002B17F
FD : Insulinorésistance; Pathologie du système nerveux; Insuline; Sensibilité; Homme; Ataxie spinocérébelleuse
FG : Hormone pancréatique; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central; Endocrinopathie; Maladie métabolique; Résistance tissu cible
ED : Insulin resistance; Nervous system diseases; Insulin; Sensitivity; Human; Spinocerebellar ataxia
EG : Pancreatic hormone; Degenerative disease; Genetic disease; Central nervous system disease; Endocrinopathy; Metabolic diseases; Target tissue resistance
SD : Resistancia insulina; Sistema nervioso patología; Insulina; Sensibilidad; Hombre; Ataxia spinocerebelosa
LO : INIST-20953.354000194841700290
ID : 10-0446317

Links to Exploration step

Pascal:10-0446317

Le document en format XML

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<div type="abstract" xml: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.</div>
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<s5>10</s5>
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<s5>37</s5>
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<s5>39</s5>
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<s0>Enfermedad hereditaria</s0>
<s5>39</s5>
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<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Endocrinopathie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Endocrinopathy</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Endocrinopatía</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Maladie métabolique</s0>
<s5>43</s5>
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<s0>Metabolic diseases</s0>
<s5>43</s5>
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<s5>44</s5>
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<NO>PASCAL 10-0446317 INIST</NO>
<ET>Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1</ET>
<AU>LALIC (Nebojša M.); DRAGASEVIC (Nataša); STEFANOVA (Elka); JOTIC (Aleksandra); LALIC (Katarina); MILICIC (Tanja); PETROVIC (Igor); MACESIC (Marija); KOSTIC (Vladimir S.)</AU>
<AF>Clinical Center of Serbia, Institute for Endocrinology, Diabetes and Metabolic Diseases/Belgrade/Serbie (1 aut., 4 aut., 5 aut., 6 aut., 8 aut.); Clinical Center of Serbia, Institute of Neurology/Belgrade/Serbie (2 aut., 3 aut., 7 aut., 9 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 12; Pp. 1976-1980; Bibl. 13 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17; 002B17F</CC>
<FD>Insulinorésistance; Pathologie du système nerveux; Insuline; Sensibilité; Homme; Ataxie spinocérébelleuse</FD>
<FG>Hormone pancréatique; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central; Endocrinopathie; Maladie métabolique; Résistance tissu cible</FG>
<ED>Insulin resistance; Nervous system diseases; Insulin; Sensitivity; Human; Spinocerebellar ataxia</ED>
<EG>Pancreatic hormone; Degenerative disease; Genetic disease; Central nervous system disease; Endocrinopathy; Metabolic diseases; Target tissue resistance</EG>
<SD>Resistancia insulina; Sistema nervioso patología; Insulina; Sensibilidad; Hombre; Ataxia spinocerebelosa</SD>
<LO>INIST-20953.354000194841700290</LO>
<ID>10-0446317</ID>
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