Association Analysis of Type 2 Diabetes Loci in Type 1 Diabetes

  1. Hui-Qi Qu1,
  2. Struan F.A. Grant23,
  3. Jonathan P. Bradfield2,
  4. Cecilia Kim2,
  5. Edward Frackelton2,
  6. Hakon Hakonarson23 and
  7. Constantin Polychronakos1
  1. 1Departments of Pediatrics and Human Genetics, McGill University, Montreal, Québec, Canada
  2. 2Center for Applied Genomics, Philadelphia, Pennsylvania
  3. 3Department of Pediatrics and Division of Human Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania
  1. Corresponding authors: Hakon Hakonarson, hakonarson{at}chop.edu, and Constantin Polychronakos, constantin.polychronakos{at}mcgill.ca

Abstract

OBJECTIVE—To search for a possible association of type 1 diabetes with 10 validated type 2 diabetes loci, i.e., PPARG, KCNJ11, WFS1, HNF1B, IDE/HHEX, SLC30A8, CDKAL1, CDKN2A/B, IGF2BP2, and FTO/RPGRIP1L.

RESEARCH DESIGN AND METHODS—Two European population samples were studied: 1) one case-control cohort of 514 type 1 diabetic subjects and 2,027 control subjects and 2) one family cohort of 483 complete type 1 diabetic case-parent trios (total 997 affected). A total of 13 tag single nucleotide polymorphisms (SNPs) from the 10 type 2 diabetes loci were analyzed for type 1 diabetes association.

RESULTS—No association of type 1 diabetes was found with any of the 10 type 2 diabetes loci, and no age-at-onset effect was detected. By combined analysis using the Wellcome Trust Case-Control Consortium type 1 diabetes data, SNP rs1412829 in the CDKN2A/B locus bordered on significance (P = 0.039) (odds ratio 0.929 [95% CI 0.867–0.995]), which did not reach the statistical significance threshold adjusted for 13 tests (α = 0.00385).

CONCLUSIONS—This study suggests that the type 2 diabetes loci do not play any obvious role in type 1 diabetes genetic susceptibility. The distinct molecular mechanisms of the two diseases highlighted the importance of differentiation diagnosis and different treatment principles.

Footnotes

  • Published ahead of print at http://diabetes.diabetesjournals.org on 21 April 2008.

    Readers may use this article as long as the work is properly cited, the use is educational and not for profit,and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted April 15, 2008.
    • Received February 24, 2008.
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  1. Published online before print April 21, 2008, doi: 10.2337/db08-0270 Diabetes July 2008 vol. 57 no. 7 1983-1986
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