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Eur J Endocrinol. 2018 Dec 1;179(6):363-372. doi: 10.1530/EJE-18-0478.

Genetic determinants of glucose levels in pregnancy: genetic risk scores analysis and GWAS in the Norwegian STORK cohort.

Author information

Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway.
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Oslo Centre for Biostatistics and Epidemiology, Oslo University Hospital, Oslo, Norway.
Department of Clinical Sciences, Clinical Research Centre, Lund University, Malmö, Sweden.
Research Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Oslo, Norway.
Finnish Institute of Molecular Medicine (FIMM), Helsinki University, Helsinki, Finland.
Department of Transplantation Medicine, Oslo University Hospital, Oslo, Norway.
University of Queensland, Diamantina Institute, Translational Research Institute, Brisbane, Australia.
Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
Norwegian National Advisory Unit on Women's Health, Oslo, Norway.


Objective Hyperglycaemia during pregnancy increases the risk of adverse health outcomes in mother and child, but the genetic aetiology is scarcely studied. Our aims were to (1) assess the overlapping genetic aetiology between the pregnant and non-pregnant population and (2) assess the importance of genome-wide polygenic contributions to glucose traits during pregnancy, by exploring whether genetic risk scores (GRSs) for fasting glucose (FG), 2-h glucose (2hG), type 2 diabetes (T2D) and BMI in non-pregnant individuals were associated with glucose measures in pregnant women. Methods We genotyped 529 Norwegian pregnant women and constructed GRS from known genome-wide significant variants and SNPs weakly associated (p > 5 × 10-8) with FG, 2hG, BMI and T2D from external genome-wide association studies (GWAS) and examined the association between these scores and glucose measures at gestational weeks 14-16 and 30-32. We also performed GWAS of FG, 2hG and shape information from the glucose curve during an oral glucose tolerance test (OGTT). Results GRSFG explained similar variance during pregnancy as in the non-pregnant population (~5%). GRSBMI and GRST2D explained up to 1.3% of the variation in the glucose traits in pregnancy. If we included variants more weakly associated with these traits, GRS2hG and GRST2D explained up to 2.4% of the variation in the glucose traits in pregnancy, highlighting the importance of polygenic contributions. Conclusions Our results suggest overlap in the genetic aetiology of FG in pregnant and non-pregnant individuals. This was less apparent with 2hG, suggesting potential differences in postprandial glucose metabolism inside and outside of pregnancy.

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