Role of the mitochondrial DNA 16184–16193 poly-C tract in type 2 diabetes
Recent evidence suggests that polymorphic genetic variation in the non-coding region of mitochondrial DNA (the 16184–16193 polycytosine [poly-C] tract) contributes to the cause of type 2 diabetes, but previous studies only just reached significance. We aimed to investigate this association. We compa...
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| Veröffentlicht in: | The Lancet (British edition) 2005-11, Vol.366 (9497), p.1650-1651 |
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| creator | Chinnery, PF Elliott, HR Patel, S Lambert, C Keers, SM Durham, SE McCarthy, MI Hitman, GA Hattersley, AT Walker, M |
| description | Recent evidence suggests that polymorphic genetic variation in the non-coding region of mitochondrial DNA (the 16184–16193 polycytosine [poly-C] tract) contributes to the cause of type 2 diabetes, but previous studies only just reached significance. We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184–16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1·16, 95% CI 0·94–1·44). Genetic variation of the 16184–16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes. |
| doi_str_mv | 10.1016/S0140-6736(05)67492-2 |
| format | Article |
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We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184–16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1·16, 95% CI 0·94–1·44). Genetic variation of the 16184–16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(05)67492-2</identifier><identifier>PMID: 16271646</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Biological and medical sciences ; Diabetes ; Diabetes Mellitus, Type 2 - genetics ; Diabetes. Impaired glucose tolerance ; DNA, Mitochondrial - genetics ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; General aspects ; Genetic diversity ; Genetics ; Humans ; Medical sciences ; Meta-Analysis as Topic ; Mitochondrial DNA ; Poly C - genetics ; Residues ; Systematic review</subject><ispartof>The Lancet (British edition), 2005-11, Vol.366 (9497), p.1650-1651</ispartof><rights>2005 Elsevier Ltd</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Lancet Ltd. 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We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184–16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1·16, 95% CI 0·94–1·44). Genetic variation of the 16184–16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes.</description><subject>Biological and medical sciences</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>General aspects</subject><subject>Genetic diversity</subject><subject>Genetics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Meta-Analysis as Topic</subject><subject>Mitochondrial DNA</subject><subject>Poly C - genetics</subject><subject>Residues</subject><subject>Systematic review</subject><issn>0140-6736</issn><issn>1474-547X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkMuKFDEUhoMoTjv6CEoQFGdRmqRyqaxkaHUUBwUv4C6kkhMmQ3WlTdJC7-YdfEOfxPR0MwNuXJ2z-P5zfj6EHlPykhIqX30llJNOql6-IOJEKq5Zx-6gBeWKd4KrH3fR4gY5Qg9KuSSEcEnEfXREJVNUcrlAH7-kCXAKuF4AXsWa3EWafY52wm8-nWIq6cD_XP1uU_d4naZtt8Q1W1dxnHHdrgEz7KMdoUJ5iO4FOxV4dJjH6Pu7t9-W77vzz2cflqfnneOM1K597pnXfpA8WE-B9-PorQtUwdh2FYLSJIgxyEExobS2PEg_8oFrYUfK-mP0fH93ndPPDZRqVrE4mCY7Q9oU03KK0oE08Ok_4GXa5Ll1M1RrMrChpw0Se8jlVEqGYNY5rmzeGkrMTrW5Vm12Hg0R5lq12bV4cji-GVfgb1MHtw14dgBscXYK2c4ulltOMU4E2XGv9xw0Z78iZFNchNmBjxlcNT7F_1T5C2oNl9M</recordid><startdate>20051105</startdate><enddate>20051105</enddate><creator>Chinnery, PF</creator><creator>Elliott, HR</creator><creator>Patel, S</creator><creator>Lambert, C</creator><creator>Keers, SM</creator><creator>Durham, SE</creator><creator>McCarthy, MI</creator><creator>Hitman, GA</creator><creator>Hattersley, AT</creator><creator>Walker, M</creator><general>Elsevier Ltd</general><general>Lancet</general><general>Elsevier Limited</general><scope>IQODW</scope><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>0TT</scope><scope>0TZ</scope><scope>0U~</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88C</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8C2</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K6X</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>KB~</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20051105</creationdate><title>Role of the mitochondrial DNA 16184–16193 poly-C tract in type 2 diabetes</title><author>Chinnery, PF ; Elliott, HR ; Patel, S ; Lambert, C ; Keers, SM ; Durham, SE ; McCarthy, MI ; Hitman, GA ; Hattersley, AT ; Walker, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-71632d9d864fad1e43bbdacf17eb43b7ff790f5bf68725799a4f6db48495ab123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Biological and medical sciences</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes. 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We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184–16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1·16, 95% CI 0·94–1·44). Genetic variation of the 16184–16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>16271646</pmid><doi>10.1016/S0140-6736(05)67492-2</doi><tpages>2</tpages></addata></record> |
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| subjects | Biological and medical sciences Diabetes Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance DNA, Mitochondrial - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance General aspects Genetic diversity Genetics Humans Medical sciences Meta-Analysis as Topic Mitochondrial DNA Poly C - genetics Residues Systematic review |
| title | Role of the mitochondrial DNA 16184–16193 poly-C tract in type 2 diabetes |
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