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Genetic Determinants of Circulating Glycine Levels and Risk of Coronary Artery Disease

Pin Huang; Johannes Kettunen; Olli Raitakari; Marjo‐Riitta Järvelin; Hooman Allayee; Jorma Viikari; Zeneng Wang; Olga Anufrieva; Nicholas C. Woodward; Janet Gukasyan; Markus Perola; Qiong Jia; Michael Boehnke; Stanley L. Hazen; Jaana A. Hartiala; Yi Han; Mika Ala‐Korpela; Markku Laakso; Terho Lehtimäki; W.H. Wilson Tang; Qin Wang; Oliver Fiehn; Karen L. Mohlke

Genetic Determinants of Circulating Glycine Levels and Risk of Coronary Artery Disease

Pin Huang
Johannes Kettunen
Olli Raitakari
Marjo‐Riitta Järvelin
Hooman Allayee
Jorma Viikari
Zeneng Wang
Olga Anufrieva
Nicholas C. Woodward
Janet Gukasyan
Markus Perola
Qiong Jia
Michael Boehnke
Stanley L. Hazen
Jaana A. Hartiala
Yi Han
Mika Ala‐Korpela
Markku Laakso
Terho Lehtimäki
W.H. Wilson Tang
Qin Wang
Oliver Fiehn
Karen L. Mohlke
Katso/Avaa
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NLM (Medline)
doi:10.1161/JAHA.119.011922
URI
https://www.ahajournals.org/doi/10.1161/JAHA.119.011922
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2021042826376
Tiivistelmä

Background: Recent studies have revealed sexually dimorphic associations between the carbamoyl‐phosphate synthase 1 locus, intermediates of the metabolic pathway leading from choline to urea, and risk of coronary artery disease (CAD) in women. Based on evidence from the literature, the atheroprotective association with carbamoyl‐phosphate synthase 1 could be mediated by the strong genetic effect of this locus on increased circulating glycine levels.

Methods and Results: We sought to identify additional genetic determinants of circulating glycine levels by carrying out a meta‐analysis of genome‐wide association study data in up to 30 118 subjects of European ancestry. Mendelian randomization and other analytical approaches were used to determine whether glycine‐associated variants were associated with CAD and traditional risk factors. Twelve loci were significantly associated with circulating glycine levels, 7 of which were not previously known to be involved in glycine metabolism (ACADM,PHGDH,COX18‐ADAMTS3,PSPH,TRIB1,PTPRD, and ABO). Glycine‐raising alleles at several loci individually exhibited directionally consistent associations with decreased risk of CAD. However, these effects could not be attributed directly to glycine because of associations with other CAD‐related traits. By comparison, genetic models that only included the 2 variants directly involved in glycine degradation and for which there were no other pleiotropic associations were not asso
ciated with risk of CAD or blood pressure, lipid levels, and obesity‐related traits.

Conclusions: These results provide additional insight into the genetic architecture of glycine metabolism, but do not yield conclusive evidence for a causal relationship between circulating levels of this amino acid and risk of CAD in humans.

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