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PubMed ID:
17463249
Public Release Type:
Journal
Publication Year: 2007
Affiliation: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
DOI:
https://doi.org/10.1126/science.1142364
Authors:
Frayling TM,
Hattersley AT,
McCarthy MI,
Wellcome Trust Case Control Consortium (WTCCC),
Doney AS,
Morris AD,
Hitman GA,
Walker M,
Cardon LR,
Knight B,
Owen KR,
Marchini JL,
Harries LW,
Weedon MN,
Zeggini E,
Groves CJ,
Ellard S,
Morris AP,
Shields B,
Barrett JC,
Freathy RM,
Rayner NW,
Perry JR,
Timpson NJ,
Lango H,
Elliott KS,
Lindgren CM
Studies:
The Finland-United States Investigation of NIDDM Genetics Study
The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set out to detect replicated diabetes association signals through analysis of 3757 additional cases and 5346 controls and by integration of our findings with equivalent data from other international consortia. We detected diabetes susceptibility loci in and around the genes CDKAL1, CDKN2A/CDKN2B, and IGF2BP2 and confirmed the recently described associations at HHEX/IDE and SLC30A8. Our findings provide insight into the genetic architecture of type 2 diabetes, emphasizing the contribution of multiple variants of modest effect. The regions identified underscore the importance of pathways influencing pancreatic beta cell development and function in the etiology of type 2 diabetes.
