Impaired Insulin Sensitivity and Secretion in Normoglycemic Patients with Spinocerebellar Ataxia Type 1
Identifieur interne : 000914 ( PascalFrancis/Corpus ); précédent : 000913; suivant : 000915Impaired 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. KosticSource :
- Movement disorders [ 0885-3185 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 10-0446317 INIST |
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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 |
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Pascal:10-0446317Le document en format XML
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<front><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>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Pancreatic hormone</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Hormona pancreática</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<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>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Metabolic diseases</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Metabolismo patología</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Résistance tissu cible</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Target tissue resistance</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Resistencia tejido blanco</s0>
<s5>44</s5>
</fC07>
<fN21><s1>291</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><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>
</server>
</inist>
</record>
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