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

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 Erdmann, Heribert Schunkert, Kay-Tee Khaw, Julian L. Griffin, Nita G. Forouhi, Robert A. Scott, Angela M. Wood, Stephen Burgess, Joanna M. M. Howson, John Danesh, Nicholas J. Wareham, Adam S. Butterworth and Claudia Langenberg ()
Additional contact information
Laura B. L. Wittemans: University of Cambridge
Luca A. Lotta: University of Cambridge
Clare Oliver-Williams: University of Cambridge
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
Fumiaki Imamura: University of Cambridge
Lingyao Zeng: Technische Universität München
Jeanette Erdmann: University of Lübeck
Heribert Schunkert: Technische Universität München
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
Joanna M. M. Howson: University of Cambridge
John Danesh: University of Cambridge
Nicholas J. Wareham: University of Cambridge
Adam S. Butterworth: University of Cambridge
Claudia Langenberg: University of Cambridge

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: 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.

Date: 2019
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-019-08936-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08936-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-019-08936-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().