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The shared allelic architecture of adiponectin levels and coronary artery disease.

Title: The shared allelic architecture of adiponectin levels and coronary artery disease.
Authors: Dastani, Zari; Johnson, Toby; Kronenberg, Florian; Nelson, Christopher P; Assimes, Themistocles L; März, Winfried; CARDIoGRAM Consortium; ADIPOGen Consortium; Richards, J Brent; Kathiresan, Sekar; Reilly, Muredach P; Samani, Nilesh J; Schunkert, Heribert; Erdmann, Jeanette; Boerwinkle, Eric; Hall, Alistair; Hengstenberg, Christian; König, Inke R; Laaksonen, Reijo; McPherson, Ruth; Thompson, John R; Thorsteinsdottir, Unnur; Ziegler, Andreas; Absher, Devin; Chen, Li; Cupples, L Adrienne; Halperin, Eran; Li, Mingyao; Musunuru, Kiran; Preuss, Michael; Schillert, Arne; Thorleifsson, Gudmar; Voight, Benjamin F; Wells, George A; Deloukas, Panos; Holm, Hilma; Roberts, Robert; Stewart, Alexandre F R; Fortmann, Stephen; Go, Alan; Hlatky, Mark; Iribarren, Carlos; Knowles, Joshua; Myers, Richard; Quertermous, Thomas; Sidney, Steven; Risch, Neil; Tang, Hua; Blankenberg, Stefan; Zeller, Tanja; Wild, Philipp; Schnabel, Renate; Sinning, Christoph; Lackner, Karl; Tiret, Laurence; Nicaud, Viviane; Cambien, Francois; Bickel, Christoph; Rupprecht, Hans J; Perret, Claire; Proust, Carole; Münzel, Thomas; Barbalic, Maja; Bis, Joshua; Chen, Ida Yii-Der; Dehghan, Abbas; Demissie-Banjaw, Serkalem; Folsom, Aaron; Glazer, Nicole; Gudnason, Vilmundur; Harris, Tamara; Heckbert, Susan; Levy, Daniel; Lumley, Thomas; Marciante, Kristin; Morrison, Alanna; O'Donnell, Christopher J; Psaty, Bruce M; Rice, Kenneth; Rotter, Jerome I; Siscovick, David S; Smith, Nicholas; Smith, Albert; Taylor, Kent D; van Duijn, Cornelia; Volcik, Kelly; Whitteman, Jaqueline; Ramachandran, Vasan; Hofman, Albert; Uitterlinden, Andre; Gretarsdottir, Solveig; Gulcher, Jeffrey R; Kong, Augustine; Stefansson, Kari; Thorgeirsson, Gudmundur; Andersen, Karl; Fischer, Marcus; Lieb, Wolfgang; Stark, Klaus; Schreiber, Stefan; Wichmann, H -Erich; Aherrahrou, Zouhair; Bruse, Petra; Doering, Angela; Illig, Thomas; Klopp, Norman; Loley, Christina; Medack, Anja; Meisinger, Christina; Meitinger, Thomas; Nahrstaedt, Janja; Peters, Annette; Willenborg, Christina; Böhm, Bernhard O; Dobnig, Harald; Grammer, Tanja B; Hoffmann, Michael M; Kleber, Marcus; Meinitzer, Andreas; Winkelmann, Bernhard R; Pilz, Stefan; Renner, Wilfried; Scharnagl, Hubert; Stojakovic, Tatjana; Tomaschitz, Andreas; Winkler, Karl; Guiducci, Candace; Burtt, Noel; Gabriel, Stacey B; Elosua, Roberto; Peltonen, Leena; Salomaa, Veikko; Schwartz, Stephen M; Melander, Olle; Altshuler, David; Dandona, Sonny; Jarinova, Olga; Qu, Liming; Wilensky, Robert; Matthai, William; Hakonarson, Hakon H; Devaney, Joe; Burnett, Mary Susan; Pichard, Augusto D; Kent, Kenneth M; Satler, Lowell; Lindsay, Joseph M; Waksman, Ron; Knouff, Christopher W; Waterworth, Dawn M; Walker, Max C; Mooser, Vincent; Epstein, Stephen E; Rader, Daniel J; Braund, Peter S; Wright, Benjamin J; Balmforth, Anthony J; Ball, Stephen G; Hall, Alistair S; Hivert, Marie-France; Timpson, Nicholas; Perry, John R B; Yuan, Xin; Scott, Robert A; Henneman, Peter; Heid, Iris M; Kizer, Jorge R; Lyytikäinen, Leo-Pekka; Fuchsberger, Christian; Tanaka, Toshiko; Morris, Andrew P; Small, Kerrin; Isaacs, Aaron; Beekman, Marian; Coassin, Stefan; Lohman, Kurt; Qi, Lu; Kanoni, Stavroula; Pankow, James S; Uh, Hae-Won; Wu, Ying; Bidulescu, Aurelian; Rasmussen-Torvik, Laura J; Greenwood, Celia M T; Ladouceur, Martin; Grimsby, Jonna; Manning, Alisa K; Liu, Ching-Ti; Kooner, Jaspal; Mooser, Vincent E; Vollenweider, Peter; Kapur, Karen A; Chambers, John; Wareham, Nicholas J; Langenberg, Claudia; Frants, Rune; Willems-vanDijk, Ko; Oostra, Ben A; Willems, Sara M; Lamina, Claudia; Winkler, Thomas W; Tracy, Russell P; Brody, Jennifer; Chen, Ida; Viikari, Jorma; Kähönen, Mika; Pramstaller, Peter P; Evans, David M; Pourcain, Beate St; Sattar, Naveed; Wood, Andrew R; Bandinelli, Stefania; Carlson, Olga D; Egan, Josephine M; Böhringer, Stefan; van Heemst, Diana; Kedenko, Lyudmyla; Kristiansson, Kati; Nuotio, Marja-Liisa; Loo, Britt-Marie; Garcia, Melissa; Kanaya, Alka; Haun, Margot; Wichmann, H Erich; Katsareli, Efi; Couper, David J; Duncan, Bruce B; Kloppenburg, Margreet; Adair, Linda S; Borja, Judith B; Wilson, James G; Musani, Solomon; Guo, Xiuqing; Semple, Robert; Teslovich, Tanya M; Allison, Matthew A; Redline, Susan; Buxbaum, Sarah G; Mohlke, Karen L; Meulenbelt, Ingrid; Ballantyne, Christie M; Dedoussis, George V; Hu, Frank B; Liu, Yongmei; Paulweber, Bernhard; Spector, Timothy D; Slagboom, P Eline; Ferrucci, Luigi; Jula, Antti; Perola, Markus; Raitakari, Olli; Florez, Jose C; Eriksson, Johan G; Frayling, Timothy M; Hicks, Andrew A; Lehtimäki, Terho; Smith, George Davey; Loos, Ruth J F; Waterworth, M; Meigs, James B; Dupuis, Josee; Richards, John Brent
Contributors: Klinik für Herz- und Kreislauferkrankungen
Publication Year: 2013
Collection: Munich University of Technology (TUM): mediaTUM
Subject Terms: info:eu-repo/classification/ddc
Description: A large body of epidemiologic data strongly suggests an association between excess adiposity and coronary artery disease (CAD). Low adiponectin levels, a hormone secreted only from adipocytes, have been associated with an increased risk of CAD in observational studies. However, these associations cannot clarify whether this relationship is causal or due to a shared set of causal factors or even confounding. Genome-wide association studies have identified common variants that influence adiponectin levels, providing valuable tools to examine the genetic relationship between adiponectin and CAD.Using 145 genome wide significant SNPs for adiponectin from the ADIPOGen consortium (n = 49,891), we tested whether adiponectin-decreasing alleles influenced risk of CAD in the CARDIoGRAM consortium (n = 85,274).In single-SNP analysis, 5 variants among 145 SNPs were associated with increased risk of CAD after correcting for multiple testing (P< 4.4 × 10(-4)). Using a multi-SNP genotypic risk score to test whether adiponectin levels and CAD have a shared genetic etiology, we found that adiponectin-decreasing alleles increased risk of CAD (P = 5.4 × 10(-7)).These findings demonstrate that adiponectin levels and CAD have a shared allelic architecture and provide rationale to undertake a Mendelian randomization studies to understand if this relationship is causal.
Document Type: article in journal/newspaper
Language: English
Relation: https://mediatum.ub.tum.de/1327947
Availability: https://mediatum.ub.tum.de/1327947
Rights: info:eu-repo/semantics/restrictedAccess
Accession Number: edsbas.2078AE3
Database: BASE