Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-12-26

AUTHORS

Kaixin Zhou, Celine Bellenguez, Chris CA Spencer, Amanda J Bennett, Ruth L Coleman, Roger Tavendale, Simon A. Hawley, Louise A Donnelly, Chris Schofield, Christopher J Groves, Lindsay Burch, Fiona Carr, Amy Strange, Colin Freeman, Jenefer M Blackwell, Elvira Bramon, Matthew A Brown, Juan P Casas, Aiden Corvin, Nicholas Craddock, Panos Deloukas, Serge Dronov, Audrey Duncanson, Sarah Edkins, Emma Gray, Sarah Hunt, Janusz Jankowski, Cordelia Langford, Hugh S Markus, Christopher G Mathew, Robert Plomin, Anna Rautanen, Stephen J Sawcer, Nilesh J Samani, Richard Trembath, Ananth C Viswanathan, Nicholas W Wood, , Lorna W Harries, Andrew T Hattersley, Alex SF Doney, Helen Colhoun, Andrew D Morris, Calum Sutherland, D. Grahame Hardie, Leena Peltonen, Mark I McCarthy, Rury R. Holman, Colin N.A. Palmer, Peter Donnelly, Ewan R Pearson, ,

ABSTRACT

Metformin is the most commonly used pharmacological therapy for type 2 diabetes. We report a genome-wide association study for glycemic response to metformin in 1,024 Scottish individuals with type 2 diabetes with replication in two cohorts including 1,783 Scottish individuals and 1,113 individuals from the UK Prospective Diabetes Study. In a combined meta-analysis, we identified a SNP, rs11212617, associated with treatment success (n = 3,920, P = 2.9 × 10(-9), odds ratio = 1.35, 95% CI 1.22-1.49) at a locus containing ATM, the ataxia telangiectasia mutated gene. In a rat hepatoma cell line, inhibition of ATM with KU-55933 attenuated the phosphorylation and activation of AMP-activated protein kinase in response to metformin. We conclude that ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin. More... »

PAGES

117-120

Journal

TITLE

Nature Genetics

ISSUE

2

VOLUME

43

Author Affiliations

  • Biomedical Research Institute, University of Dundee, DD1 9SY, UK
  • UK Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford, OX3 7BN, UK
  • Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, UK
  • Diabetes Trials Unit, University of Oxford, UK
  • College of Life Sciences, University of Dundee, UK
  • Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Cambridge CB2 0XY, UK
  • The South London and Maudsley NHS Foundation Trust, Denmark Hill, London SE5 8AF, UK
  • Diamantina Institute of Cancer, Immunology and Metabolic Medicine, Princess Alexandra Hospital, University of Queensland, Brisbane, Queensland, Australia
  • Dept Epidemiology and Public Health, University College London, WC1E 6BT, UK
  • Neuropsychiatric Genetics Research Group, Institute of Molecular Medicine, Trinity College Dublin, Dublin 2, Eire
  • Dept Psychological Medicine, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK
  • Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK
  • Molecular and Physiological Sciences, The Wellcome Trust, London, NW1 2BE, UK
  • Department of Clinical Pharmacology, Old Road Campus, University of Oxford, Oxford OX3 7DQ, UK
  • Clinical Neurosciences, St George’s University of London, London SW17 0RE
  • Department of Medical and Molecular Genetics, King’s College London School of Medicine, Guy’s Hospital, London SE1 9RT, UK
  • King’s College London Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Denmark Hill, London SE5 8AF, UK
  • University of Cambridge Dept Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK
  • Dept Cardiovascular Science, University of Leicester, Glenfield Hospital, Leicester LE3 9QP
  • NIHR Biomedical Research Centre for Ophthalmology, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London EC1V 2PD, UK
  • Dept Molecular Neuroscience, Institute of Neurology, Queen Square, London WC1N 3BG, UK
  • Peninsula College of Medicine and Dentistry, University of Exeter, UK
  • Ninewells Hospital & Medical School, Dundee, UK
  • UK Oxford National Institute for Health Research Biomedical Research Centre, Churchill Hospital, Old Road Headington, Oxford, UK
  • Department of Statistics, University of Oxford, South Parks Road, Oxford OX1 3TG, UK
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ng.735

    DOI

    http://dx.doi.org/10.1038/ng.735

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1000086491

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/21186350


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    31 schema:description Metformin is the most commonly used pharmacological therapy for type 2 diabetes. We report a genome-wide association study for glycemic response to metformin in 1,024 Scottish individuals with type 2 diabetes with replication in two cohorts including 1,783 Scottish individuals and 1,113 individuals from the UK Prospective Diabetes Study. In a combined meta-analysis, we identified a SNP, rs11212617, associated with treatment success (n = 3,920, P = 2.9 × 10(-9), odds ratio = 1.35, 95% CI 1.22-1.49) at a locus containing ATM, the ataxia telangiectasia mutated gene. In a rat hepatoma cell line, inhibition of ATM with KU-55933 attenuated the phosphorylation and activation of AMP-activated protein kinase in response to metformin. We conclude that ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin.
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