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Nat Commun. 2019 Mar 5;10(1):1060. doi: 10.1038/s41467-019-08936-1.

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

Author information

1
MRC Epidemiology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK.
2
MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, CB1 8RN, UK.
3
Homerton College, Hills Road, Cambridge, CB2 8PH, UK.
4
NIHR BRC Nutritional Biomarker Laboratory, University of Cambridge, Cambridge, CB2 0QQ, UK.
5
Deutsches Herzzentrum München, Technische Universität München, München, 80636, Germany.
6
DZHK, Partner Site München Heart Alliance, München, 80802, Germany.
7
Institute for Cardiogenetics, University of Lübeck, Lübeck, 23562, Germany.
8
DZHK, partner site Hamburg/Lübeck/Kiel, Lübeck, 23562, Germany.
9
University Heart Center Lübeck, Lübeck, 23562, Germany.
10
Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge, Cambridge, CB2 0SR, UK.
11
Biochemistry Department, University of Cambridge, Cambridge, CB2 1QW, UK.
12
MRC Biostatistics Unit, University of Cambridge, Cambridge, CB2 0SR, UK.
13
Wellcome Sanger Institute, Genome Campus, Hinxton, CB10 1SA, UK.
14
MRC Epidemiology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK. Claudia.Langenberg@mrc-epid.cam.ac.uk.

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.

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