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dc.contributor.authorWaterworth, Dawn
dc.contributor.authorO'Rahilly, Stephen
dc.contributor.authorHivert, Marie-France
dc.contributor.authorLoos, Ruth J. F.
dc.contributor.authorTanaka, Toshiko
dc.contributor.authorTimpson, Nicholas John
dc.contributor.authorSemple, Robert K.
dc.contributor.authorSoranzo, Nicole
dc.contributor.authorSong, Kijoung
dc.contributor.authorRocha, Nuno
dc.contributor.authorGrundberg, Elin
dc.contributor.authorDupuis, Josée
dc.contributor.authorLangenberg, Claudia
dc.contributor.authorProkopenko, Inga
dc.contributor.authorSladek, Robert
dc.contributor.authorAulchenko, Yurii
dc.contributor.authorWaeber, Gerard
dc.contributor.authorErdmann, Jeanette
dc.contributor.authorBurnett, Mary-Susan
dc.contributor.authorSattar, Naveed
dc.contributor.authorDevaney, Joseph
dc.contributor.authorWillenborg, Christina
dc.contributor.authorHingorani, Aroon
dc.contributor.authorWitteman, Jaquelin C. M.
dc.contributor.authorVollenweider, Peter
dc.contributor.authorGlaser, Beate
dc.contributor.authorHengstenberg, Christian
dc.contributor.authorFerrucci, Luigi
dc.contributor.authorMelzer, David
dc.contributor.authorStark, Klaus
dc.contributor.authorDeanfield, John
dc.contributor.authorWinogradow, Janina
dc.contributor.authorGrassl, Martina
dc.contributor.authorHall, Alistair S.
dc.contributor.authorEgan, Josephine M.
dc.contributor.authorRicketts, Sally L.
dc.contributor.authorKönig, Inke R.
dc.contributor.authorReinhard, Wibke
dc.contributor.authorGrundy, Scott
dc.contributor.authorWichmann, H-Erich
dc.contributor.authorBarter, Phil
dc.contributor.authorMahley, Robert
dc.contributor.authorKesaniemi, Y. Antero
dc.contributor.authorRader, Daniel J.
dc.contributor.authorReilly, Muredach P.
dc.contributor.authorStewart, Alexandre F. R.
dc.contributor.authorVan Duijn, Cornelia M.
dc.contributor.authorSchunkert, Heribert
dc.contributor.authorBurling, Keith
dc.contributor.authorDeloukas, Panos
dc.contributor.authorPastinen, Tomi
dc.contributor.authorSamani, Nilesh J.
dc.contributor.authorMcPherson, Ruth
dc.contributor.authorDavey Smith, George
dc.contributor.authorFrayling, Timothy M.
dc.contributor.authorWareham, Nicholas J.
dc.contributor.authorMooser, Vincent
dc.contributor.authorSpector, Tim D.
dc.contributor.authorRichards, J. Brent
dc.contributor.authorFlorez, Jose Carlos
dc.contributor.authorPerry, John R.B.
dc.contributor.authorSaxena, Richa
dc.contributor.authorEvans, David
dc.contributor.authorMeigs, James Benjamin
dc.contributor.authorThompson, John R.
dc.contributor.authorEpstein, Stephen E.
dc.date.accessioned2011-04-23T00:54:32Z
dc.date.issued2009
dc.identifier.citationRichards, J. Brent, Dawn Waterworth, Stephen O'Rahilly, Marie-France Hivert, Ruth J. F. Loos, John R. B. Perry, Toshiko Tanaka, et al. 2009. A genome-wide association study reveals variants in ARL15 that influence adiponectin levels. PLoS Genetics 5(12): e1000768.en_US
dc.identifier.issn1553-7390en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:4874764
dc.description.abstractThe 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 = 9.2×10−19 for 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 muscle. These findings identify a novel protein, ARL15, which influences circulating adiponectin levels and may impact upon CHD risk.en_US
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofdoi:10.1371/journal.pgen.1000768en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781107/pdf/en_US
dash.licenseLAA
dc.subjectcardiovascular disordersen_US
dc.subjectcongenital heart diseaseen_US
dc.subjectdiabetes and endocrinologyen_US
dc.subjectobesityen_US
dc.subjecttype 2 diabetesen_US
dc.subjectgenetics and genomicsen_US
dc.subjectgenetics of diseaseen_US
dc.titleA Genome-Wide Association Study Reveals Variants in ARL15 that Influence Adiponectin Levelsen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalPLoS Geneticsen_US
dash.depositing.authorMeigs, James Benjamin
dc.date.available2011-04-23T00:54:32Z
dash.affiliation.otherHMS^Medicine-Massachusetts General Hospitalen_US
dash.affiliation.otherHMS^Anaesthesia-Massachusetts General Hospitalen_US
dash.affiliation.otherHMS^Medicine-Massachusetts General Hospitalen_US
dc.identifier.doi10.1371/journal.pgen.1000768*
dash.authorsorderedfalse
dash.contributor.affiliatedFlorez, Jose
dash.contributor.affiliatedMeigs, James
dash.contributor.affiliatedSaxena, Richa


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