Predisposing genetic factors for diabetic polyneuropathy in patients with type 1 diabetes: a population-based case-control study
Oxidative stress plays a key role in the development of microvascular complications of diabetes mellitus (DM). Antioxidant enzymes protect against the rapid onset of diabetic polyneuropathy (DPN) by reducing oxidative stress. Genetic variations that affect activity or expression levels of the antiox...
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| Veröffentlicht in: | Acta diabetologica 2003-12, Vol.40 Suppl 2, p.S375-s379 |
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| container_title | Acta diabetologica |
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| creator | Strokov, I A Bursa, T R Drepa, O I Zotova, E V Nosikov, V V Ametov, A S |
| description | Oxidative stress plays a key role in the development of microvascular complications of diabetes mellitus (DM). Antioxidant enzymes protect against the rapid onset of diabetic polyneuropathy (DPN) by reducing oxidative stress. Genetic variations that affect activity or expression levels of the antioxidant enzymes may therefore be associated with susceptibility to DPN. We examined polymorphic markers Ala(-9)Val in SOD2 gene and Arg213Gly in SOD3 gene for possible relation to DPN in Russian type 1 diabetic patients. Four hundred Russian white patients with type 1 diabetes were studied using neurological examination according to recommendations of the San Antonio Conference on Diabetic Neuropathy. Two groups were formed from the general sample. Definition of frequency distribution of the polymorphic markers was performed in these groups using the polymerase chain reaction. Genes encoding the enzymes Mn-SOD and extracellular superoxide dismutase (EC-SOD) were found to be associated with the pathogenesis of DPN. |
| doi_str_mv | 10.1007/s00592-003-0123-x |
| format | Article |
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Antioxidant enzymes protect against the rapid onset of diabetic polyneuropathy (DPN) by reducing oxidative stress. Genetic variations that affect activity or expression levels of the antioxidant enzymes may therefore be associated with susceptibility to DPN. We examined polymorphic markers Ala(-9)Val in SOD2 gene and Arg213Gly in SOD3 gene for possible relation to DPN in Russian type 1 diabetic patients. Four hundred Russian white patients with type 1 diabetes were studied using neurological examination according to recommendations of the San Antonio Conference on Diabetic Neuropathy. Two groups were formed from the general sample. Definition of frequency distribution of the polymorphic markers was performed in these groups using the polymerase chain reaction. 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Antioxidant enzymes protect against the rapid onset of diabetic polyneuropathy (DPN) by reducing oxidative stress. Genetic variations that affect activity or expression levels of the antioxidant enzymes may therefore be associated with susceptibility to DPN. We examined polymorphic markers Ala(-9)Val in SOD2 gene and Arg213Gly in SOD3 gene for possible relation to DPN in Russian type 1 diabetic patients. Four hundred Russian white patients with type 1 diabetes were studied using neurological examination according to recommendations of the San Antonio Conference on Diabetic Neuropathy. Two groups were formed from the general sample. Definition of frequency distribution of the polymorphic markers was performed in these groups using the polymerase chain reaction. Genes encoding the enzymes Mn-SOD and extracellular superoxide dismutase (EC-SOD) were found to be associated with the pathogenesis of DPN.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetic Neuropathies - epidemiology</subject><subject>Diabetic Neuropathies - genetics</subject><subject>European Continental Ancestry Group</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genotype</subject><subject>Glycated Hemoglobin A - analysis</subject><subject>Humans</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>Russia</subject><subject>Smoking</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkU2LFDEQhoMo7jj6A7xI8OAtWvma7niTxS9Y0IOeQzqp3s3S02mTNLt986ebdQYED5UqwvO-VPIS8pLDWw7QvSsA2ggGIBlwIdn9I7LjSgqmhZSPyQ6MAqaVMBfkWSm30KBO9k_JBVcdqL4TO_L7e8YQy5JKnK_pNc5Yo6ej8zXlQseUaYhu-Hu5pGmbcc1pcfVmo3GmbYg410LvYr2hdVuQ8jOP5T11TbKsU4PSzAZXMFDfTubTXHOaaKlr2J6TJ6ObCr449z35-enjj8sv7Orb56-XH66Ylxoqc-7ADUfvhsH0OhyUcgfv9aixUwNAr0YTlJCogzRde_KhFXjtgwgYvBRyT96cfJecfq1Yqj3G4nGa3IxpLbbjGnjfvnJPXv8H3qY1z203y43uleGCN4ifIJ9TKRlHu-R4dHmzHOxDNvaUjW2G9iEbe980r87G63DE8E9xDkP-AYHTjHc</recordid><startdate>20031201</startdate><enddate>20031201</enddate><creator>Strokov, I A</creator><creator>Bursa, T R</creator><creator>Drepa, O I</creator><creator>Zotova, E V</creator><creator>Nosikov, V V</creator><creator>Ametov, A S</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20031201</creationdate><title>Predisposing genetic factors for diabetic polyneuropathy in patients with type 1 diabetes: a population-based case-control study</title><author>Strokov, I A ; 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Antioxidant enzymes protect against the rapid onset of diabetic polyneuropathy (DPN) by reducing oxidative stress. Genetic variations that affect activity or expression levels of the antioxidant enzymes may therefore be associated with susceptibility to DPN. We examined polymorphic markers Ala(-9)Val in SOD2 gene and Arg213Gly in SOD3 gene for possible relation to DPN in Russian type 1 diabetic patients. Four hundred Russian white patients with type 1 diabetes were studied using neurological examination according to recommendations of the San Antonio Conference on Diabetic Neuropathy. Two groups were formed from the general sample. Definition of frequency distribution of the polymorphic markers was performed in these groups using the polymerase chain reaction. Genes encoding the enzymes Mn-SOD and extracellular superoxide dismutase (EC-SOD) were found to be associated with the pathogenesis of DPN.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>14704872</pmid><doi>10.1007/s00592-003-0123-x</doi></addata></record> |
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| subjects | Adolescent Adult Case-Control Studies Child Diabetes Mellitus, Type 1 - genetics Diabetic Neuropathies - epidemiology Diabetic Neuropathies - genetics European Continental Ancestry Group Genetic Predisposition to Disease - genetics Genotype Glycated Hemoglobin A - analysis Humans Middle Aged Polymorphism, Single Nucleotide Risk Factors Russia Smoking |
| title | Predisposing genetic factors for diabetic polyneuropathy in patients with type 1 diabetes: a population-based case-control study |
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