OBJECTIVE: Common variants at the 2q36.3-IRS1 locus are associated with insulin resistance (IR), type 2 diabetes (T2D) and coronary artery disease (CAD) in large-scale association studies. We tested the hypothesis that variants at this locus are associated with subclinical atherosclerosis traits. METHODS: We studied 2740 Framingham Heart Study participants (54.9% women; mean age 57.8 years) with measures of coronary artery or abdominal aortic calcium, internal and common carotid intima-media thickness, and ankle-brachial index (ABI). We tested 1) four SNPs previously shown to be associated with IR (rs2972146, rs2943650), T2D (rs2943641) or CAD (rs2943634) and 2) any SNP at 2q36.3-IRS1, for association with subclinical atherosclerosis traits, adjusting for atherosclerosis risk factors. We set type 1 error rate for test 1) as 0.05/5 traits = P < 0.01, and for test 2) as 0.05 divided by the effective number of independent tests, divided by 5 for the number of traits analyzed. RESULTS: We found no association between the four known SNPs and subclinical atherosclerosis, but identified one SNP (rs10167219, r(2) with rs2943634 = 0.07) at 2q36.3 that was significantly associated with ABI (corrected P = 0.009). However, rs10167219 was not associated with ABI (P = 0.70) in 35,404 participants in a published ABI association study. CONCLUSION: Common variants at the 2q36.3-IRS1 locus were not associated with subclinical atherosclerosis traits in this study which was adequately powered to find associations with moderate effect size. Although IR and T2D may be mechanistically linked to CAD via subclinical atherosclerosis, an alternate mechanism for the IR-T2D-CAD associations at 2q36.3-IRS1 must be postulated.
OBJECTIVE: Common variants at the 2q36.3-IRS1 locus are associated with insulin resistance (IR), type 2 diabetes (T2D) and coronary artery disease (CAD) in large-scale association studies. We tested the hypothesis that variants at this locus are associated with subclinical atherosclerosis traits. METHODS: We studied 2740 Framingham Heart Study participants (54.9% women; mean age 57.8 years) with measures of coronary artery or abdominal aortic calcium, internal and common carotid intima-media thickness, and ankle-brachial index (ABI). We tested 1) four SNPs previously shown to be associated with IR (rs2972146, rs2943650), T2D (rs2943641) or CAD (rs2943634) and 2) any SNP at 2q36.3-IRS1, for association with subclinical atherosclerosis traits, adjusting for atherosclerosis risk factors. We set type 1 error rate for test 1) as 0.05/5 traits = P < 0.01, and for test 2) as 0.05 divided by the effective number of independent tests, divided by 5 for the number of traits analyzed. RESULTS: We found no association between the four known SNPs and subclinical atherosclerosis, but identified one SNP (rs10167219, r(2) with rs2943634 = 0.07) at 2q36.3 that was significantly associated with ABI (corrected P = 0.009). However, rs10167219 was not associated with ABI (P = 0.70) in 35,404 participants in a published ABI association study. CONCLUSION: Common variants at the 2q36.3-IRS1 locus were not associated with subclinical atherosclerosis traits in this study which was adequately powered to find associations with moderate effect size. Although IR and T2D may be mechanistically linked to CAD via subclinical atherosclerosis, an alternate mechanism for the IR-T2D-CAD associations at 2q36.3-IRS1 must be postulated.
Authors: Christopher J O'Donnell; Maryam Kavousi; Albert V Smith; Sharon L R Kardia; Mary F Feitosa; Shih-Jen Hwang; Yan V Sun; Michael A Province; Thor Aspelund; Abbas Dehghan; Udo Hoffmann; Lawrence F Bielak; Qunyuan Zhang; Gudny Eiriksdottir; Cornelia M van Duijn; Caroline S Fox; Mariza de Andrade; Aldi T Kraja; Sigurdur Sigurdsson; Suzette E Elias-Smale; Joanne M Murabito; Lenore J Launer; Aad van der Lugt; Sekar Kathiresan; Gabriel P Krestin; David M Herrington; Timothy D Howard; Yongmei Liu; Wendy Post; Braxton D Mitchell; Jeffrey R O'Connell; Haiqing Shen; Alan R Shuldiner; David Altshuler; Roberto Elosua; Veikko Salomaa; Stephen M Schwartz; David S Siscovick; Benjamin F Voight; Joshua C Bis; Nicole L Glazer; Bruce M Psaty; Eric Boerwinkle; Gerardo Heiss; Stefan Blankenberg; Tanja Zeller; Philipp S Wild; Renate B Schnabel; Arne Schillert; Andreas Ziegler; Thomas F Münzel; Charles C White; Jerome I Rotter; Michael Nalls; Matthijs Oudkerk; Andrew D Johnson; Anne B Newman; Andre G Uitterlinden; Joseph M Massaro; Julie Cunningham; Tamara B Harris; Albert Hofman; Patricia A Peyser; Ingrid B Borecki; L Adrienne Cupples; Vilmundur Gudnason; Jacqueline C M Witteman Journal: Circulation Date: 2011-12-05 Impact factor: 29.690
Authors: Philip Greenland; Joseph S Alpert; George A Beller; Emelia J Benjamin; Matthew J Budoff; Zahi A Fayad; Elyse Foster; Mark A Hlatky; John McB Hodgson; Frederick G Kushner; Michael S Lauer; Leslee J Shaw; Sidney C Smith; Allen J Taylor; William S Weintraub; Nanette K Wenger; Alice K Jacobs Journal: Circulation Date: 2010-11-15 Impact factor: 29.690
Authors: Nathan D Wong; Victor A Lopez; Matthew Allison; Robert C Detrano; Roger S Blumenthal; Aaron R Folsom; Pamela Ouyang; Michael H Criqui Journal: Atherosclerosis Date: 2010-09-18 Impact factor: 5.162
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Authors: Cristina Alonso-Bouzón; Laure Carcaillon; Francisco J García-García; María S Amor-Andrés; Mariam El Assar; Leocadio Rodríguez-Mañas Journal: Age (Dordr) Date: 2014-02
Authors: Paul Welsh; David Preiss; Suzanne M Lloyd; Anton J de Craen; J Wouter Jukema; Rudi G Westendorp; Brendan M Buckley; Patricia M Kearney; Andrew Briggs; David J Stott; Ian Ford; Naveed Sattar Journal: Diabetologia Date: 2014-09-30 Impact factor: 10.122
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