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1. KCND3 potassium channel gene variant confers susceptibility to electrocardiographic early repolarization pattern

Author

Teumer, A. (Alexander), Trenkwalder, T. (Teresa), Kessler, T. (Thorsten), Jamshidi, Y. (Yalda), Berg, M.E. (Marten) van den, Kaess, B. (Bernhard), Nelson, C.P. (Christopher P.), Bastiaenen, R. (Rachel), de Bortoli, M. (Marzia), Rossini, A. (Alessandra), Deisenhofer, I. (Isabel), Stark, K. (Klaus), Assa, S. (Solmaz), Braund, P.S. (Peter), Cabrera, C. (Claudia), Dominiczak, A.F. (Anna F.), Gögele, M. (Martin), Hall, L.M. (Leanne M.), Ikram, M.A. (Arfan), Kavousi, M. (Maryam), Lackner, K.J. (Karl), Study, L.C. (Lifelines Cohort), Müller, C., Münzel, T. (Thomas), Nauck, M. (Matthias), Padmanabhan, S. (Sandosh), Pfeiffer, A.F.H. (Andreas), Spector, T.D. (Timothy), Uitterlinden, A.G. (André), Verweij, N. (Niek), Völker, U. (Uwe), Warren, H. (Helen), Zafar, M. (Mobeen), Felix, S.B. (Stephan), Kors, J.A. (Jan), Snieder, H. (Harold), Munroe, P. (Patricia), Penninx, B.W.J.H., Fuchsberger, C. (Christian), Schmidt, G. (Georg), Nolte, I.M. (Ilja), Schunkert, H. (Heribert), Pramstaller, P.P. (Peter Paul), Wild, P.S. (Philipp), Harst, P. (Pim) van der, Stricker, B.H.Ch. (Bruno), Schnabel, R.B. (Renate), Samani, N.J. (Nilesh), Hengstenberg, C. (Christian), Dörr, M. (Marcus), Behr, E.R. (Elijah), Reinhard, W. (Wibke), Teumer, A. (Alexander), Trenkwalder, T. (Teresa), Kessler, T. (Thorsten), Jamshidi, Y. (Yalda), Berg, M.E. (Marten) van den, Kaess, B. (Bernhard), Nelson, C.P. (Christopher P.), Bastiaenen, R. (Rachel), de Bortoli, M. (Marzia), Rossini, A. (Alessandra), Deisenhofer, I. (Isabel), Stark, K. (Klaus), Assa, S. (Solmaz), Braund, P.S. (Peter), Cabrera, C. (Claudia), Dominiczak, A.F. (Anna F.), Gögele, M. (Martin), Hall, L.M. (Leanne M.), Ikram, M.A. (Arfan), Kavousi, M. (Maryam), Lackner, K.J. (Karl), Study, L.C. (Lifelines Cohort), Müller, C., Münzel, T. (Thomas), Nauck, M. (Matthias), Padmanabhan, S. (Sandosh), Pfeiffer, A.F.H. (Andreas), Spector, T.D. (Timothy), Uitterlinden, A.G. (André), Verweij, N. (Niek), Völker, U. (Uwe), Warren, H. (Helen), Zafar, M. (Mobeen), Felix, S.B. (Stephan), Kors, J.A. (Jan), Snieder, H. (Harold), Munroe, P. (Patricia), Penninx, B.W.J.H., Fuchsberger, C. (Christian), Schmidt, G. (Georg), Nolte, I.M. (Ilja), Schunkert, H. (Heribert), Pramstaller, P.P. (Peter Paul), Wild, P.S. (Philipp), Harst, P. (Pim) van der, Stricker, B.H.Ch. (Bruno), Schnabel, R.B. (Renate), Samani, N.J. (Nilesh), Hengstenberg, C. (Christian), Dörr, M. (Marcus), Behr, E.R. (Elijah), and Reinhard, W. (Wibke)

Abstract

BACKGROUND: The presence of an early repolarization pattern (ERP) on the surface ECG is associated with risk of ventricular fibrillation and sudden cardiac death. Family studies have shown that ERP is a highly heritable trait, but molecular genetic determinants are unknown. METHODS: To identify genetic susceptibility loci for ERP, we performed a GWAS and meta-analysis in 2,181 cases and 23,641 controls of European ancestry. RESULTS. We identified a genome-wide significant (P < 5 × 10-8) locus in the potassium voltage-gated channel subfamily D member 3 (KCND3) gene that was successfully replicated in additional 1,124 cases and 12,510 controls. A subsequent joint meta-analysis of the discovery and replication cohorts identified rs1545300 as the lead SNP at the KCND3 locus (OR 0.82 per minor T allele, P = 7.7 × 10-12) but did not reveal additional loci. Colocalization analyses indicate causal effects of KCND3 gene expression levels on ERP in both cardiac left ventricle and tibial artery. CONCLUSIONS: In this study, we identified for the first time to our knowledge a genome-wide significant association of a genetic variant with ERP. Our findings of a locus in the KCND3 gene provide insights not only into the genetic determinants but also into the pathophysiological mechanism of ERP, discovering a promising candidate for functional studies.

Published
2019
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2. A genome-wide association study reveals variants in ARL15 that influence adiponectin levels

Author

Richards, J.B. (Brent), Waterworth, D. (Dawn), O'Rahilly, S. (Stephen), Hivert, M.-F. (Marie-France), Loos, R.J.F. (Ruth), Perry, J.R.B. (John), Tanaka, T. (Toshiko), Timpson, N.J. (Nicholas), Semple, R.K. (Robert), Soranzo, N. (Nicole), Song, K. (Kijoung), Rocha, N. (Nuno), Grundberg, E. (Elin), Dupuis, J. (Josée), Florez, J.C. (Jose), Langenberg, C. (Claudia), Prokopenko, I. (Inga), Saxena, R. (Richa), Sladek, R. (Rob), Aulchenko, Y.S. (Yurii), Evans, D.M. (David), Waeber, G. (Gérard), Burnett, M.S., Sattar, N. (Naveed), Devaney, J. (Joseph), Willenborg, C. (Christina), Hingorani, A. (Aroon), Witteman, J.C.M. (Jacqueline), Vollenweider, P. (Peter), Glaser, B. (Beate), Hengstenberg, C. (Christian), Ferrucci, L. (Luigi), Melzer, D. (David), Stark, K. (Klaus), Deanfield, J. (John), Winogradow, J. (Janina), Grassl, M. (Martina), Hall, A.S. (Alistair), Egan, J.M. (Josephine), Thompson, J.R. (John), Ricketts, S.L. (Sally), König, I.R. (Inke), Reinhard, W. (Wibke), Grundy, S.M. (Scott), Wichmann, H.E. (Heinz Erich), Barter, P. (Phil), Mahley, R. (Robert), Kesaniemi, Y.A. (Antero), Rader, D.J. (Daniel), Reilly, M.P. (Muredach), Epstein, S.E. (Stephen), Stewart, A.F.R. (Alexandre), Tikka-Kleemola, P. (Päivi), Schunkert, H. (Heribert), Burling, K.A. (Keith), Erdmann, J. (Jeanette), Deloukas, P. (Panagiotis), Pastinen, T. (Tomi), Samani, N.J. (Nilesh), McPherson, R. (Ruth), Smith, A.V. (Davey), Frayling, T.M. (Timothy), Wareham, N.J. (Nick), Meigs, J.B. (James), Mooser, V. (Vincent), Spector, T.D. (Timothy), Richards, J.B. (Brent), Waterworth, D. (Dawn), O'Rahilly, S. (Stephen), Hivert, M.-F. (Marie-France), Loos, R.J.F. (Ruth), Perry, J.R.B. (John), Tanaka, T. (Toshiko), Timpson, N.J. (Nicholas), Semple, R.K. (Robert), Soranzo, N. (Nicole), Song, K. (Kijoung), Rocha, N. (Nuno), Grundberg, E. (Elin), Dupuis, J. (Josée), Florez, J.C. (Jose), Langenberg, C. (Claudia), Prokopenko, I. (Inga), Saxena, R. (Richa), Sladek, R. (Rob), Aulchenko, Y.S. (Yurii), Evans, D.M. (David), Waeber, G. (Gérard), Burnett, M.S., Sattar, N. (Naveed), Devaney, J. (Joseph), Willenborg, C. (Christina), Hingorani, A. (Aroon), Witteman, J.C.M. (Jacqueline), Vollenweider, P. (Peter), Glaser, B. (Beate), Hengstenberg, C. (Christian), Ferrucci, L. (Luigi), Melzer, D. (David), Stark, K. (Klaus), Deanfield, J. (John), Winogradow, J. (Janina), Grassl, M. (Martina), Hall, A.S. (Alistair), Egan, J.M. (Josephine), Thompson, J.R. (John), Ricketts, S.L. (Sally), König, I.R. (Inke), Reinhard, W. (Wibke), Grundy, S.M. (Scott), Wichmann, H.E. (Heinz Erich), Barter, P. (Phil), Mahley, R. (Robert), Kesaniemi, Y.A. (Antero), Rader, D.J. (Daniel), Reilly, M.P. (Muredach), Epstein, S.E. (Stephen), Stewart, A.F.R. (Alexandre), Tikka-Kleemola, P. (Päivi), Schunkert, H. (Heribert), Burling, K.A. (Keith), Erdmann, J. (Jeanette), Deloukas, P. (Panagiotis), Pastinen, T. (Tomi), Samani, N.J. (Nilesh), McPherson, R. (Ruth), Smith, A.V. (Davey), Frayling, T.M. (Timothy), Wareham, N.J. (Nick), Meigs, J.B. (James), Mooser, V. (Vincent), and Spector, T.D. (Timothy)

Abstract

The adipocyte-derived protein adiponectin is highly heritable and inversely associated with risk of type 2 diabetes mellitus (T2D) and coronary heart disease (CHD). We meta-analyzed 3 genome-wide association studies for circulating adiponectin levels (n = 8,531) and sought validation of the lead single nucleotide polymorphisms (SNPs) in 5 additional cohorts (n = 6,202). Five SNPs were genome-wide significant in their relationship with adiponectin (P≤5×10-8). We then tested whether these 5 SNPs were associated with risk of T2D and CHD using a Bonferroni-corrected threshold of P≤0.011 to declare statistical significance for these disease associations. SNPs at the adiponectin-encoding ADIPOQ locus demonstrated the strongest associations with adiponectin levels (P-combined = 9.2×10-19for lead SNP, rs266717, n = 14,733). A novel variant in the ARL15 (ADP-ribosylation factor-like 15) gene was associated with lower circulating levels of adiponectin (rs4311394-G, P-combined = 2.9×10-8, n = 14,733). This same risk allele at ARL15 was also associated with a higher risk of CHD (odds ratio [OR] = 1.12, P = 8.5×10-6, n = 22,421) more nominally, an increased risk of T2D (OR = 1.11, P = 3.2×10-3, n = 10,128), and several metabolic traits. Expression studies in humans indicated that ARL15 is well-expressed in skeletal

Published
2009
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