<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Scott RA</submitter><funding>NCATS NIH HHS</funding><funding>British Heart Foundation</funding><funding>NCRR NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>Medical Research Council</funding><funding>NHLBI NIH HHS</funding><funding>NHGRI NIH HHS</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Novo Nordisk Fonden</funding><pagination>1291-6</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3331745</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>61(5)</volume><pubmed_abstract>Gene-lifestyle interactions have been suggested to contribute to the development of type 2 diabetes. Glucose levels 2 h after a standard 75-g glucose challenge are used to diagnose diabetes and are associated with both genetic and lifestyle factors. However, whether these factors interact to determine 2-h glucose levels is unknown. We meta-analyzed single nucleotide polymorphism (SNP) × BMI and SNP × physical activity (PA) interaction regression models for five SNPs previously associated with 2-h glucose levels from up to 22 studies comprising 54,884 individuals without diabetes. PA levels were dichotomized, with individuals below the first quintile classified as inactive (20%) and the remainder as active (80%). BMI was considered a continuous trait. Inactive individuals had higher 2-h glu</pubmed_abstract><journal>Diabetes</journal><pubmed_title>No interactions between previously associated 2-hour glucose gene variants and physical activity or BMI on 2-hour glucose levels.</pubmed_title><pmcid>PMC3331745</pmcid><funding_grant_id>MC_U147585824</funding_grant_id><funding_grant_id>U1475000001</funding_grant_id><funding_grant_id>U1475000002</funding_grant_id><funding_grant_id>G0600717</funding_grant_id><funding_grant_id>RG/07/008/23674</funding_grant_id><funding_grant_id>P30 DK020572</funding_grant_id><funding_grant_id>T32 HL007575</funding_grant_id><funding_grant_id>UL1 RR025741</funding_grant_id><funding_grant_id>R01 DK072041</funding_grant_id><funding_grant_id>T32 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YD</pubmed_authors><pubmed_authors>Siscovick DS</pubmed_authors><pubmed_authors>Rice K</pubmed_authors><pubmed_authors>Dowling NF</pubmed_authors><pubmed_authors>Stancakova A</pubmed_authors><pubmed_authors>Tonjes A</pubmed_authors><pubmed_authors>Kao WH</pubmed_authors><pubmed_authors>Bornstein SR</pubmed_authors><pubmed_authors>Forouhi NG</pubmed_authors><pubmed_authors>Groop L</pubmed_authors><pubmed_authors>Walker M</pubmed_authors><pubmed_authors>Loos RJ</pubmed_authors><pubmed_authors>Hivert MF</pubmed_authors><pubmed_authors>Pankow JS</pubmed_authors><pubmed_authors>Scott RA</pubmed_authors><pubmed_authors>Laakso M</pubmed_authors><pubmed_authors>Bergmann S</pubmed_authors><pubmed_authors>Collins FS</pubmed_authors><pubmed_authors>Franks PW</pubmed_authors><pubmed_authors>Bouatia-Naji N</pubmed_authors><pubmed_authors>Jackson AU</pubmed_authors><pubmed_authors>Carlson OD</pubmed_authors><pubmed_authors>Sandholt CH</pubmed_authors><pubmed_authors>Fox 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AK</pubmed_authors><pubmed_authors>Dennison EM</pubmed_authors><pubmed_authors>Lyssenko V</pubmed_authors><pubmed_authors>Rotter JI</pubmed_authors><pubmed_authors>Dupuis J</pubmed_authors><pubmed_authors>Boerwinkle E</pubmed_authors><pubmed_authors>Chu AY</pubmed_authors><pubmed_authors>Williams GH</pubmed_authors><pubmed_authors>Stumvoll M</pubmed_authors><pubmed_authors>Jonsson A</pubmed_authors><pubmed_authors>Prokopenko I</pubmed_authors><pubmed_authors>Wood AR</pubmed_authors><pubmed_authors>Ferrucci L</pubmed_authors><pubmed_authors>Shungin D</pubmed_authors><pubmed_authors>Gustafsson S</pubmed_authors><pubmed_authors>Hallmans G</pubmed_authors><pubmed_authors>Marques-Vidal P</pubmed_authors><pubmed_authors>Lecoeur C</pubmed_authors><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Xie W</pubmed_authors><pubmed_authors>Barroso I</pubmed_authors><pubmed_authors>Hu FB</pubmed_authors><pubmed_authors>Erdos MR</pubmed_authors><pubmed_authors>Chen 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F</pubmed_authors><pubmed_authors>Hansen T</pubmed_authors><pubmed_authors>Marmot M</pubmed_authors><pubmed_authors>Sayer AA</pubmed_authors><pubmed_authors>Jameson KA</pubmed_authors><pubmed_authors>Jorgensen T</pubmed_authors><pubmed_authors>Glazer NL</pubmed_authors><pubmed_authors>Aadahl M</pubmed_authors><pubmed_authors>Cooper C</pubmed_authors><pubmed_authors>Froguel P</pubmed_authors><pubmed_authors>Holloway JW</pubmed_authors><pubmed_authors>Kumari M</pubmed_authors><pubmed_authors>North KE</pubmed_authors></additional><is_claimable>false</is_claimable><name>No interactions between previously associated 2-hour glucose gene variants and physical activity or BMI on 2-hour glucose levels.</name><description>Gene-lifestyle interactions have been suggested to contribute to the development of type 2 diabetes. Glucose levels 2 h after a standard 75-g glucose challenge are used to diagnose diabetes and are associated with both genetic and lifestyle factors. However, whether these factors interact to determine 2-h glucose levels is unknown. We meta-analyzed single nucleotide polymorphism (SNP) × BMI and SNP × physical activity (PA) interaction regression models for five SNPs previously associated with 2-h glucose levels from up to 22 studies comprising 54,884 individuals without diabetes. PA levels were dichotomized, with individuals below the first quintile classified as inactive (20%) and the remainder as active (80%). BMI was considered a continuous trait. Inactive individuals had higher 2-h glu</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2026-04-29T23:13:14.292Z</modification><creation>2026-04-21T03:09:02.291Z</creation></dates><accession>S-EPMC3331745</accession><cross_references><pubmed>22415877</pubmed><doi>10.2337/db11-0973</doi></cross_references></HashMap>