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Nature GeNetics VOLUME 42 | NUMBER 7 | JULY 2010 579 A rt i c l e s
 

Summary: Nature GeNetics VOLUME 42 | NUMBER 7 | JULY 2010 579
A rt i c l e s
Bycombininggenome-wideassociationdatafrom8,130individualswithtype2diabetes(T2D)and38,987controlsof
Europeandescentandfollowinguppreviouslyunidentifiedmeta-analysissignalsinafurther34,412casesand59,925controls,
weidentified12newT2DassociationsignalswithcombinedP<510-8.Theseincludeasecondindependentsignalatthe
KCNQ1locus;thefirstreport,toourknowledge,ofanX-chromosomalassociation(nearDUSP9);andafurtherinstanceof
overlapbetweenlociimplicatedinmonogenicandmultifactorialformsofdiabetes(atHNF1A).Theidentifiedlociaffectboth
beta-cellfunctionandinsulinaction,and,overall,T2Dassociationsignalsshowevidenceofenrichmentforgenesinvolvedin
cellcycleregulation.WealsoshowthatahighproportionofT2Dsusceptibilitylociharborindependentassociationsignals
influencingapparentlyunrelatedcomplextraits.
Type 2 diabetes (T2D) is characterized by insulin resistance and
deficient beta-cell function1. The escalating prevalence of T2D and
the limitations of currently available preventative and therapeutic
options highlight the need for a more complete understanding of
T2D pathogenesis. To date, approximately 25 genome-wide significant
common variant associations with T2D have been described, mostly
through genome-wide association (GWA) analyses213. The identities
of the variants and genes mediating the susceptibility effects at most
of these signals have yet to be established, and the known variants
account for less than 10% of the overall estimated genetic contribution

  

Source: Abecasis, Goncalo - Department of Biostatistics, University of Michigan

 

Collections: Biology and Medicine; Mathematics