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Assessing the causal association of glycine with risk of cardio-metabolic diseases

Author

Listed:
  • Laura B. L. Wittemans

    (University of Cambridge)

  • Luca A. Lotta

    (University of Cambridge)

  • Clare Oliver-Williams

    (University of Cambridge
    Homerton College)

  • Isobel D. Stewart

    (University of Cambridge)

  • Praveen Surendran

    (University of Cambridge)

  • Savita Karthikeyan

    (University of Cambridge)

  • Felix R. Day

    (University of Cambridge)

  • Albert Koulman

    (University of Cambridge
    University of Cambridge)

  • Fumiaki Imamura

    (University of Cambridge)

  • Lingyao Zeng

    (Technische Universität München
    Partner Site München Heart Alliance)

  • Jeanette Erdmann

    (University of Lübeck
    partner site Hamburg/Lübeck/Kiel
    University Heart Center Lübeck)

  • Heribert Schunkert

    (Technische Universität München
    Partner Site München Heart Alliance)

  • Kay-Tee Khaw

    (University of Cambridge)

  • Julian L. Griffin

    (University of Cambridge)

  • Nita G. Forouhi

    (University of Cambridge)

  • Robert A. Scott

    (University of Cambridge)

  • Angela M. Wood

    (University of Cambridge)

  • Stephen Burgess

    (University of Cambridge
    University of Cambridge)

  • Joanna M. M. Howson

    (University of Cambridge)

  • John Danesh

    (University of Cambridge
    Wellcome Sanger Institute)

  • Nicholas J. Wareham

    (University of Cambridge)

  • Adam S. Butterworth

    (University of Cambridge)

  • Claudia Langenberg

    (University of Cambridge)

Abstract

Circulating levels of glycine have previously been associated with lower incidence of coronary heart disease (CHD) and type 2 diabetes (T2D) but it remains uncertain if glycine plays an aetiological role. We present a meta-analysis of genome-wide association studies for glycine in 80,003 participants and investigate the causality and potential mechanisms of the association between glycine and cardio-metabolic diseases using genetic approaches. We identify 27 genetic loci, of which 22 have not previously been reported for glycine. We show that glycine is genetically associated with lower CHD risk and find that this may be partly driven by blood pressure. Evidence for a genetic association of glycine with T2D is weaker, but we find a strong inverse genetic effect of hyperinsulinaemia on glycine. Our findings strengthen evidence for a protective effect of glycine on CHD and show that the glycine-T2D association may be driven by a glycine-lowering effect of insulin resistance.

Suggested Citation

  • Laura B. L. Wittemans & Luca A. Lotta & Clare Oliver-Williams & Isobel D. Stewart & Praveen Surendran & Savita Karthikeyan & Felix R. Day & Albert Koulman & Fumiaki Imamura & Lingyao Zeng & Jeanette E, 2019. "Assessing the causal association of glycine with risk of cardio-metabolic diseases," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08936-1
    DOI: 10.1038/s41467-019-08936-1
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