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Christine Sommer, Anne K Jenum, Christin W Waage, Kjersti Mørkrid, Line Sletner and Kåre I Birkeland

Objective

To explore the differences between Europeans and South Asians in BMI, subcutaneous fat, and serum leptin (s-leptin) levels during and after pregnancy and their relationship with gestational diabetes (GDM).

Design

Multi-ethnic population-based cohort study, whereof 353 Europeans (93.1% of the included) and 190 South Asians (95.0% of the included).

Methods

S-leptin, BMI, and subcutaneous fat (sum of triceps, subscapular, and suprailiac skinfolds) were measured at 14 and 28 weeks of gestation, and 14 weeks after delivery. GDM was diagnosed with the WHO criteria 2013.

Results

South Asians had similar thickness of the triceps and suprailiac skinfolds, thicker subscapular skinfold, and higher s-leptin than Europeans in early pregnancy, despite lower BMI. South Asians retained more subcutaneous fat (mean (95% CI) 10.0 (7.4–12.7) mm vs 3.8 (1.9–5.8) mm) and BMI (1.5 (1.2–1.8) kg/m2 vs 0.1 (−0.1 to 0.3) kg/m2) than Europeans 14 weeks after delivery and s-leptin decreased less in South Asians than Europeans (−0.13 (−0.27 to −0.00) μg/l vs −0.47 (−0.57 to −0.37) μg/l, P<0.001 for all). The prevalence of GDM was 23.8% (n=84) in Europeans and 42.6% (n=81) in South Asians. BMI, subcutaneous fat, and s-leptin were all positively associated with GDM, also after adjustment for covariates.

Conclusions

The relatively high amounts of subcutaneous fat and s-leptin in South Asians in early pregnancy contributed to their increased risk of GDM. South Asians retained more weight and subcutaneous fat after delivery, potentially increasing their risk of adiposity and GDM in future pregnancies.

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Gunn-Helen Moen, Christine Sommer, Rashmi B Prasad, Line Sletner, Leif Groop, Elisabeth Qvigstad and Kåre I Birkeland

Objective

To summarize the current knowledge on epigenetic alterations in mother and offspring subjected to gestational diabetes (GDM) and indicate future topics for research.

Design

Systematic review.

Methods

We performed extensive searches in PubMed, EMBASE and Google scholar, using a combination of the search terms: GDM, gestational diabetes, epigenetic(s), methylation, histone modification, histone methylation, histone acetylation, microRNA and miRNA. Studies that compared women diagnosed with GDM and healthy controls were included. Two authors independently scanned the abstracts, and all included papers were read by at least two authors. The searches were completed on October 31st, 2016.

Results

We identified 236 articles, of which 43 were considered relevant for this systematic review. Studies published showed that epigenetic alterations could be found in both mothers with GDM and their offspring. However, differences in methodology, diagnostic criteria for GDM and populations studied, together with a limited number of published studies and small sample sizes, preclude clear conclusions about the role of epigenetic modifications in transmitting risk from GDM mothers to their offspring.

Conclusion

The current research literature suggests that GDM may have impact on epigenetic modifications in the mother and offspring. However, larger studies that include multiple cohorts of GDM patients and their offspring are needed.

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Gunn-Helen Moen, Marissa LeBlanc, Christine Sommer, Rashmi B Prasad, Tove Lekva, Kjersti R Normann, Elisabeth Qvigstad, Leif Groop, Kåre I Birkeland, David M Evans and Kathrine F Frøslie

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.