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Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes
Aims/hypothesis There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contribut...
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| Published in: | Diabetologia 2012-02, Vol.55 (2), p.340-348 |
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| container_issue | 2 |
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| container_title | Diabetologia |
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| creator | Snogdal, L. S. Wod, M. Grarup, N. Vestmar, M. Sparsø, T. Jørgensen, T. Lauritzen, T. Beck-Nielsen, H. Henriksen, J. E. Pedersen, O. Hansen, T. Højlund, K. |
| description | Aims/hypothesis
There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contributes to type 2 diabetes susceptibility or influences diabetes-related metabolic traits.
Methods
OxPhos gene variants (
n
= 10) that had been nominally associated (
p
|
| doi_str_mv | 10.1007/s00125-011-2377-0 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_912806465</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>912806465</sourcerecordid><originalsourceid>FETCH-LOGICAL-c443t-605ad52ef3205313f3761a7d9aed6ef6f79bd41b140676f92d084969655f83ae3</originalsourceid><addsrcrecordid>eNp1kVuLFDEQhYMo7uzqD_BFgiD71Fq5dudRBm-w4IuCb02mu7Jm6O7MprqXnX9vhh5dEHwIuZzvVIo6jL0S8E4A1O8JQEhTgRCVVHVdwRO2EVrJCrRsnrLNSa5EY39esEuiPQAoo-1zdiElOCOV27C7bRrHNPF7n6OfYznFiaeH2JfLPfLDr0Rl5eOwirc4IfFIfEoz93z0-5R55xdCnkKx0jIUf0aKNPupK6-Zz8cDcsn76Hc4I71gz4IfCF-e9yv249PH79sv1c23z1-3H26qTms1VxaM743EoCQYJVRQtRW-7p3H3mKwoXa7Xoud0GBrG5zsodHOOmtMaJRHdcWu17qHnO4WpLkdI3U4DH7CtFDrhGzAamsK-eYfcp-WPJXmTpB2xilVILFCXU5EGUN7yHH0-dgKaE9ptGsabUmjPaXRQvG8PhdediP2fx1_xl-At2fAU-eHkMvMIj1yxtTCgCicXDkq0nSL-bHD___-G-_NocU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>912495933</pqid></control><display><type>article</type><title>Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes</title><source>Springer Link</source><creator>Snogdal, L. S. ; Wod, M. ; Grarup, N. ; Vestmar, M. ; Sparsø, T. ; Jørgensen, T. ; Lauritzen, T. ; Beck-Nielsen, H. ; Henriksen, J. E. ; Pedersen, O. ; Hansen, T. ; Højlund, K.</creator><creatorcontrib>Snogdal, L. S. ; Wod, M. ; Grarup, N. ; Vestmar, M. ; Sparsø, T. ; Jørgensen, T. ; Lauritzen, T. ; Beck-Nielsen, H. ; Henriksen, J. E. ; Pedersen, O. ; Hansen, T. ; Højlund, K.</creatorcontrib><description>Aims/hypothesis
There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contributes to type 2 diabetes susceptibility or influences diabetes-related metabolic traits.
Methods
OxPhos gene variants (
n
= 10) that had been nominally associated (
p
< 0.01) with type 2 diabetes in a recent genome-wide meta-analysis (
n
= 10,108) were selected for follow-up in 3,599 type 2 diabetic and 4,956 glucose-tolerant Danish individuals. A meta-analysis of these variants was performed in 11,729 type 2 diabetic patients and 43,943 non-diabetic individuals. The impact on OGTT-derived metabolic traits was evaluated in 5,869 treatment-naive individuals from the Danish Inter99 study.
Results
The minor alleles of
COX10
rs9915302 (
p
= 0.02) and
COX5B
rs1466100 (
p
= 0.005) showed nominal association with type 2 diabetes in our Danish cohort. However, in the meta-analysis, none of the investigated variants showed a robust association with type 2 diabetes after correction for multiple testing. Among the alleles potentially associated with type 2 diabetes, none negatively influenced surrogate markers of insulin sensitivity in non-diabetic participants, while the minor alleles of
UQCRC1
rs2228561 and
COX10
rs10521253 showed a weak (
p
< 0.01 to
p
< 0.05) negative influence on indices of glucose-stimulated insulin secretion.
Conclusions/interpretation
We cannot rule out the possibility that common variants in or near OxPhos genes may influence beta cell function in non-diabetic individuals. However, our quantitative trait studies and a sufficiently large meta-analysis indicate that common variation in proximity to the examined OxPhos genes is not a major cause of insulin resistance or type 2 diabetes.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-011-2377-0</identifier><identifier>PMID: 22095239</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Alleles ; Biological and medical sciences ; Body fat ; Case-Control Studies ; Denmark ; Diabetes ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes. Impaired glucose tolerance ; Electron Transport Complex IV - genetics ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Genetic Variation ; Genomes ; Glucose ; Glucose - metabolism ; Health sciences ; Human Physiology ; Humans ; Hypotheses ; Influence ; Insulin Resistance ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Meta-analysis ; Metabolic Diseases ; Metabolism ; Metabolites ; Mitochondria - metabolism ; Models, Biological ; Models, Genetic ; Musculoskeletal system ; Oxidative Phosphorylation ; Oxygen - chemistry ; Pathogenesis ; Phosphorylation ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci</subject><ispartof>Diabetologia, 2012-02, Vol.55 (2), p.340-348</ispartof><rights>Springer-Verlag 2011</rights><rights>2015 INIST-CNRS</rights><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-605ad52ef3205313f3761a7d9aed6ef6f79bd41b140676f92d084969655f83ae3</citedby><cites>FETCH-LOGICAL-c443t-605ad52ef3205313f3761a7d9aed6ef6f79bd41b140676f92d084969655f83ae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25571501$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22095239$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Snogdal, L. S.</creatorcontrib><creatorcontrib>Wod, M.</creatorcontrib><creatorcontrib>Grarup, N.</creatorcontrib><creatorcontrib>Vestmar, M.</creatorcontrib><creatorcontrib>Sparsø, T.</creatorcontrib><creatorcontrib>Jørgensen, T.</creatorcontrib><creatorcontrib>Lauritzen, T.</creatorcontrib><creatorcontrib>Beck-Nielsen, H.</creatorcontrib><creatorcontrib>Henriksen, J. E.</creatorcontrib><creatorcontrib>Pedersen, O.</creatorcontrib><creatorcontrib>Hansen, T.</creatorcontrib><creatorcontrib>Højlund, K.</creatorcontrib><title>Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contributes to type 2 diabetes susceptibility or influences diabetes-related metabolic traits.
Methods
OxPhos gene variants (
n
= 10) that had been nominally associated (
p
< 0.01) with type 2 diabetes in a recent genome-wide meta-analysis (
n
= 10,108) were selected for follow-up in 3,599 type 2 diabetic and 4,956 glucose-tolerant Danish individuals. A meta-analysis of these variants was performed in 11,729 type 2 diabetic patients and 43,943 non-diabetic individuals. The impact on OGTT-derived metabolic traits was evaluated in 5,869 treatment-naive individuals from the Danish Inter99 study.
Results
The minor alleles of
COX10
rs9915302 (
p
= 0.02) and
COX5B
rs1466100 (
p
= 0.005) showed nominal association with type 2 diabetes in our Danish cohort. However, in the meta-analysis, none of the investigated variants showed a robust association with type 2 diabetes after correction for multiple testing. Among the alleles potentially associated with type 2 diabetes, none negatively influenced surrogate markers of insulin sensitivity in non-diabetic participants, while the minor alleles of
UQCRC1
rs2228561 and
COX10
rs10521253 showed a weak (
p
< 0.01 to
p
< 0.05) negative influence on indices of glucose-stimulated insulin secretion.
Conclusions/interpretation
We cannot rule out the possibility that common variants in or near OxPhos genes may influence beta cell function in non-diabetic individuals. However, our quantitative trait studies and a sufficiently large meta-analysis indicate that common variation in proximity to the examined OxPhos genes is not a major cause of insulin resistance or type 2 diabetes.</description><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Body fat</subject><subject>Case-Control Studies</subject><subject>Denmark</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Electron Transport Complex IV - genetics</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Genetic Variation</subject><subject>Genomes</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Health sciences</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Influence</subject><subject>Insulin Resistance</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Meta-analysis</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mitochondria - metabolism</subject><subject>Models, Biological</subject><subject>Models, Genetic</subject><subject>Musculoskeletal system</subject><subject>Oxidative Phosphorylation</subject><subject>Oxygen - chemistry</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Quantitative Trait Loci</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp1kVuLFDEQhYMo7uzqD_BFgiD71Fq5dudRBm-w4IuCb02mu7Jm6O7MprqXnX9vhh5dEHwIuZzvVIo6jL0S8E4A1O8JQEhTgRCVVHVdwRO2EVrJCrRsnrLNSa5EY39esEuiPQAoo-1zdiElOCOV27C7bRrHNPF7n6OfYznFiaeH2JfLPfLDr0Rl5eOwirc4IfFIfEoz93z0-5R55xdCnkKx0jIUf0aKNPupK6-Zz8cDcsn76Hc4I71gz4IfCF-e9yv249PH79sv1c23z1-3H26qTms1VxaM743EoCQYJVRQtRW-7p3H3mKwoXa7Xoud0GBrG5zsodHOOmtMaJRHdcWu17qHnO4WpLkdI3U4DH7CtFDrhGzAamsK-eYfcp-WPJXmTpB2xilVILFCXU5EGUN7yHH0-dgKaE9ptGsabUmjPaXRQvG8PhdediP2fx1_xl-At2fAU-eHkMvMIj1yxtTCgCicXDkq0nSL-bHD___-G-_NocU</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Snogdal, L. S.</creator><creator>Wod, M.</creator><creator>Grarup, N.</creator><creator>Vestmar, M.</creator><creator>Sparsø, T.</creator><creator>Jørgensen, T.</creator><creator>Lauritzen, T.</creator><creator>Beck-Nielsen, H.</creator><creator>Henriksen, J. E.</creator><creator>Pedersen, O.</creator><creator>Hansen, T.</creator><creator>Højlund, K.</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20120201</creationdate><title>Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes</title><author>Snogdal, L. S. ; Wod, M. ; Grarup, N. ; Vestmar, M. ; Sparsø, T. ; Jørgensen, T. ; Lauritzen, T. ; Beck-Nielsen, H. ; Henriksen, J. E. ; Pedersen, O. ; Hansen, T. ; Højlund, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-605ad52ef3205313f3761a7d9aed6ef6f79bd41b140676f92d084969655f83ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>Body fat</topic><topic>Case-Control Studies</topic><topic>Denmark</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Electron Transport Complex IV - genetics</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Genetic Variation</topic><topic>Genomes</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Health sciences</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Influence</topic><topic>Insulin Resistance</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Meta-analysis</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Mitochondria - metabolism</topic><topic>Models, Biological</topic><topic>Models, Genetic</topic><topic>Musculoskeletal system</topic><topic>Oxidative Phosphorylation</topic><topic>Oxygen - chemistry</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Quantitative Trait Loci</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Snogdal, L. S.</creatorcontrib><creatorcontrib>Wod, M.</creatorcontrib><creatorcontrib>Grarup, N.</creatorcontrib><creatorcontrib>Vestmar, M.</creatorcontrib><creatorcontrib>Sparsø, T.</creatorcontrib><creatorcontrib>Jørgensen, T.</creatorcontrib><creatorcontrib>Lauritzen, T.</creatorcontrib><creatorcontrib>Beck-Nielsen, H.</creatorcontrib><creatorcontrib>Henriksen, J. E.</creatorcontrib><creatorcontrib>Pedersen, O.</creatorcontrib><creatorcontrib>Hansen, T.</creatorcontrib><creatorcontrib>Højlund, K.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Snogdal, L. S.</au><au>Wod, M.</au><au>Grarup, N.</au><au>Vestmar, M.</au><au>Sparsø, T.</au><au>Jørgensen, T.</au><au>Lauritzen, T.</au><au>Beck-Nielsen, H.</au><au>Henriksen, J. E.</au><au>Pedersen, O.</au><au>Hansen, T.</au><au>Højlund, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>55</volume><issue>2</issue><spage>340</spage><epage>348</epage><pages>340-348</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contributes to type 2 diabetes susceptibility or influences diabetes-related metabolic traits.
Methods
OxPhos gene variants (
n
= 10) that had been nominally associated (
p
< 0.01) with type 2 diabetes in a recent genome-wide meta-analysis (
n
= 10,108) were selected for follow-up in 3,599 type 2 diabetic and 4,956 glucose-tolerant Danish individuals. A meta-analysis of these variants was performed in 11,729 type 2 diabetic patients and 43,943 non-diabetic individuals. The impact on OGTT-derived metabolic traits was evaluated in 5,869 treatment-naive individuals from the Danish Inter99 study.
Results
The minor alleles of
COX10
rs9915302 (
p
= 0.02) and
COX5B
rs1466100 (
p
= 0.005) showed nominal association with type 2 diabetes in our Danish cohort. However, in the meta-analysis, none of the investigated variants showed a robust association with type 2 diabetes after correction for multiple testing. Among the alleles potentially associated with type 2 diabetes, none negatively influenced surrogate markers of insulin sensitivity in non-diabetic participants, while the minor alleles of
UQCRC1
rs2228561 and
COX10
rs10521253 showed a weak (
p
< 0.01 to
p
< 0.05) negative influence on indices of glucose-stimulated insulin secretion.
Conclusions/interpretation
We cannot rule out the possibility that common variants in or near OxPhos genes may influence beta cell function in non-diabetic individuals. However, our quantitative trait studies and a sufficiently large meta-analysis indicate that common variation in proximity to the examined OxPhos genes is not a major cause of insulin resistance or type 2 diabetes.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22095239</pmid><doi>10.1007/s00125-011-2377-0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0012-186X |
| ispartof | Diabetologia, 2012-02, Vol.55 (2), p.340-348 |
| issn | 0012-186X 1432-0428 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_912806465 |
| source | Springer Link |
| subjects | Alleles Biological and medical sciences Body fat Case-Control Studies Denmark Diabetes Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetes. Impaired glucose tolerance Electron Transport Complex IV - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Genetic Variation Genomes Glucose Glucose - metabolism Health sciences Human Physiology Humans Hypotheses Influence Insulin Resistance Internal Medicine Medical sciences Medicine Medicine & Public Health Meta-analysis Metabolic Diseases Metabolism Metabolites Mitochondria - metabolism Models, Biological Models, Genetic Musculoskeletal system Oxidative Phosphorylation Oxygen - chemistry Pathogenesis Phosphorylation Polymorphism, Single Nucleotide Quantitative Trait Loci |
| title | Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes |
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