Genetic association analysis of LARS2 with type 2 diabetes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-10-22

AUTHORS

E. Reiling, B. Jafar-Mohammadi, E. van ’t Riet, M. N. Weedon, J. V. van Vliet-Ostaptchouk, T. Hansen, R. Saxena, T. W. van Haeften, P. A. Arp, S. Das, G. Nijpels, M. J. Groenewoud, E. C. van Hove, A. G. Uitterlinden, J. W. A. Smit, A. D. Morris, A. S. F. Doney, C. N. A. Palmer, C. Guiducci, A. T. Hattersley, T. M. Frayling, O. Pedersen, P. E. Slagboom, D. M. Altshuler, L. Groop, J. A. Romijn, J. A. Maassen, M. H. Hofker, J. M. Dekker, M. I. McCarthy, L. M. ’t Hart

ABSTRACT

Aims/hypothesisLARS2 has been previously identified as a potential type 2 diabetes susceptibility gene through the low-frequency H324Q (rs71645922) variant (minor allele frequency [MAF] 3.0%). However, this association did not achieve genome-wide levels of significance. The aim of this study was to establish the true contribution of this variant and common variants in LARS2 (MAF > 5%) to type 2 diabetes risk.MethodsWe combined genome-wide association data (n = 10,128) from the DIAGRAM consortium with independent data derived from a tagging single nucleotide polymorphism (SNP) approach in Dutch individuals (n = 999) and took forward two SNPs of interest to replication in up to 11,163 Dutch participants (rs17637703 and rs952621). In addition, because inspection of genome-wide association study data identified a cluster of low-frequency variants with evidence of type 2 diabetes association, we attempted replication of rs9825041 (a proxy for this group) and the previously identified H324Q variant in up to 35,715 participants of European descent.ResultsNo association between the common SNPs in LARS2 and type 2 diabetes was found. Our replication studies for the two low-frequency variants, rs9825041 and H324Q, failed to confirm an association with type 2 diabetes in Dutch, Scandinavian and UK samples (OR 1.03 [95% CI 0.95–1.12], p = 0.45, n = 31,962 and OR 0.99 [0.90–1.08], p = 0.78, n = 35,715 respectively).Conclusions/interpretationIn this study, the largest study examining the role of sequence variants in LARS2 in type 2 diabetes susceptibility, we found no evidence to support previous data indicating a role in type 2 diabetes susceptibility. More... »

PAGES

103

References to SciGraph publications

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  • Journal

    TITLE

    Diabetologia

    ISSUE

    1

    VOLUME

    53

    Author Affiliations

  • Department of Molecular Cell Biology, Leiden University Medical Center (LUMC), P.O. Box 9600, 2300RC, Leiden, the Netherlands
  • National Institute for Health Research, Oxford Biomedical Research Centre, University of Oxford, Oxford, UK
  • Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, the Netherlands
  • Diabetes Genetics Institute of Biomedical and Clinical Science, Peninsula Medical School, Exeter, UK
  • Molecular Genetics, Medical Biology Section, Department of Pathology and Medical Biology, University Medical Centre Groningen and University of Groningen, Groningen, the Netherlands
  • Faculty of Health Science, University of Southern Denmark, Odense, Denmark
  • Program in Medical and Population Genetics, Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA
  • Department of Internal Medicine, University Medical Center Utrecht, Utrecht, the Netherlands
  • Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, the Netherlands
  • Oxford Center for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
  • Department of General Practice, VU University Medical Center, Amsterdam, the Netherlands
  • Department of Endocrinology, Leiden University Medical Center, Leiden, the Netherlands
  • Diabetes Research Group, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK
  • Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark
  • Department of Medical Statistics, Leiden University Medical Center, Leiden, the Netherlands
  • Department of Genetics, Harvard Medical School, Boston, MA, USA
  • Department of Medicine, Helsinki University Hospital, University of Helsinki, Helsinki, Finland
  • Department of Endocrinology, VU Medical Center, Amsterdam, the Netherlands
  • Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00125-009-1557-7

    DOI

    http://dx.doi.org/10.1007/s00125-009-1557-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1001376188

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/19847392


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    512 schema:name Department of Clinical Sciences, University Hospital Malmö, Clinical Research Center, Lund University, Malmö, Sweden
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