Genetics of Glucose regulation in Gestation and Growth (Gen3G): a prospective prebirth cohort of mother–child pairs in Sherbrooke, Canada

Guillemette, Laetitia; Allard, Catherine; Lacroix, Marilyn; Patenaude, Johane; Battista, Marie-Claude; Doyon, Myriam; Moreau, Julie; Ménard, Julie; Bouchard, Luigi; Ardilouze, Jean-Luc; Perron, Patrice; Hivert, Marie‐France

doi:10.1136/bmjopen-2015-010031

Cited by 72 publications

(85 citation statements)

References 31 publications

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“…The Genetics of Glucose regulation in Gestation and Growth (Gen3G) cohort is a prospective pregnancy study that has been previously described in detail (4–6). The ethics committee at Centre Hospitalier Universitaire de Sherbrooke approved the study; participants gave written informed consent.…”

Section: Methodsmentioning

confidence: 99%

Heterogeneous Contribution of Insulin Sensitivity and Secretion Defects to Gestational Diabetes Mellitus

et al. 2016

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OBJECTIVETo characterize physiologic subtypes of gestational diabetes mellitus (GDM).RESEARCH DESIGN AND METHODSInsulin sensitivity and secretion were estimated in 809 women at 24–30 weeks' gestation, using oral glucose tolerance test–based indices. In women with GDM (8.3%), defects in insulin sensitivity or secretion were defined below the 25th percentile in women with normal glucose tolerance (NGT). GDM subtypes were defined based on the defect(s) present.RESULTSRelative to women with NGT, women with predominant insulin sensitivity defects (51% of GDM) had higher BMI and fasting glucose, larger infants (birth weight z score 0.57 [−0.01 to 1.37] vs. 0.03 [−0.53 to 0.52], P = 0.001), and greater risk of GDM-associated adverse outcomes (57.6 vs. 28.2%, P = 0.003); differences were independent of BMI. Women with predominant insulin secretion defects (30% of GDM) had BMI, fasting glucose, infant birth weights, and risk of adverse outcomes similar to those in women with NGT.CONCLUSIONSHeterogeneity of physiologic processes underlying hyperglycemia exists among women with GDM. GDM with impaired insulin sensitivity confers a greater risk of adverse outcomes.

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Section: Methodsmentioning

confidence: 99%

Heterogeneous Contribution of Insulin Sensitivity and Secretion Defects to Gestational Diabetes Mellitus

et al. 2016

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“…Mother and infant pairs were participants in the Genetics of Glucose Regulation in Gestation and Growth (Gen3G), a prospective pre-birth cohort recruited at the Center Hospitalier Universitaire de Sherbrooke (CHUS) in Canada, described in detail previously 16 . Expecting mothers were recruited during the first trimester of pregnancy and were eligible for the study if they were 18 y of age or older, had a singleton pregnancy, and were not diagnosed with pre-pregnancy diabetes or diabetes during the first trimester.…”

Section: Methodsmentioning

confidence: 99%

Validation of a DNA methylation reference panel for the estimation of nucleated cells types in cord blood

et al. 2016

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Cord blood is widely used as surrogate tissue in epigenome-wide association studies of prenatal conditions. Cell type composition variation across samples can be an important confounder of epigenome-wide association studies in blood that constitute a mixture of cells. We evaluated a newly developed cord blood reference panel to impute cell type composition from DNA methylation levels, including nucleated red blood cells (nRBCs). We estimated cell type composition from 154 unique cord blood samples with available DNA methylation data as well as direct measurements of nucleated cell types. We observed high correlations between the estimated and measured composition for nRBCs (r = 0.92, R2 = 0.85), lymphocytes (r = 0.77, R2 = 0.58), and granulocytes (r = 0.72, R2 = 0.52), and a moderate correlation for monocytes (r = 0.51, R2 = 0.25) as well as relatively low root mean square errors from the residuals ranging from 1.4 to 5.4%. These results validate the use of the cord blood reference panel and highlight its utility and limitations for epidemiological studies.

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“…From 2010 to 2013, we enrolled pregnant women receiving care at the Centre hospitalier universitaire de Sherbrooke (CHUS) [12]. The CHUS ethics board approved our project, and each participant provided signed informed consent.…”

Section: Methodsmentioning

confidence: 99%

“…We performed anthropometry measurements using standardized procedures and calculated BMI [12]. Pregravid self-reported weight and weight measured in the 1st trimester were strongly correlated ( r = 0.99, p < 0.0001).…”

Section: Methodsmentioning

confidence: 99%

“…Within 72 h of delivery, we measured the triceps, biceps, subscapular, and suprailiac skinfold thicknesses (SFTs). We obtained the consent of 265 mothers to measure SFTs in neonates, performed with a calibrated skinfold caliper (AMG Medical Inc., Montreal, QC, Canada) [12] in duplicate on the right side of the neonate, lying on her/his left side. The sum of the 4 SFTs was used as an indicator for total neonatal adiposity.…”

Section: Methodsmentioning

confidence: 99%

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Associations of Maternal Leptin with Neonatal Adiposity Differ according to Pregravid Weight

Patenaude

Lacerte²,

Lacroix³

et al. 2017

Neonatology

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Background: During pregnancy, maternal circulating leptin is released by maternal adipose tissue and the placenta, and may have a role infetal development. Objectives: We investigated maternal leptinemia and glycemia associations with neonatal adiposity, taking into account pregravid weight status. Methods: We included 235 pregnant women from the Genetics of Glucose Regulation in Gestation and Growth prospective cohort with data: blood samples collected during the 2nd trimester, an oral glucose tolerance test (OGTT), and the measured leptin and glucose levels. As an integrated measure of maternal leptin exposure, we calculated the area under the curve for maternal leptin at the OGTT (AUC_leptin). Within 72 h of delivery, we measured the triceps, biceps, subscapular, and suprailiac skinfold thicknesses (SFTs); the sum of these SFTs represented neonatal adiposity. We conducted a regression analysis to assess the maternal metabolic determinants of neonatal adiposity, adjusting for parity, smoking status, maternal triglyceride levels, gestational weight gain, placental weight, delivery mode, neonate sex, and gestational age at delivery. Results: The pregravid BMI of the participating women was 23.3 (21.2-27.0). In the 2nd trimester, maternal AUC_leptin was 1,292.0 (767.0-2,222.5) (ng × min)/mL, and fasting glucose levels were 4.2 ± 0.4 mmol/L. At delivery, the neonatal sum of 4 SFTs was 17.9 ± 3.3 mm. Higher maternal leptinemia was associated with higher neonatal adiposity (β = 4.23 mm [SE = 1.77] per log-AUC_leptin; p = 0.02) in mothers with a BMI ≥25, independently of confounders and maternal glycemia, but not in mothers with a BMI <25. Higher maternal fasting glucose was associated with higher neonatal adiposity (β = 0.88 mm [SE = 0.30] per SD glucose; p = 0.005) in mothers with a BMI <25, independently of confounders and maternal leptinemia. Conclusion: Maternal leptinemia may be associated with neonatal adiposity in offspring from overweight/obese mothers, independently of maternal glycemia.

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Genetics of Glucose regulation in Gestation and Growth (Gen3G): a prospective prebirth cohort of mother–child pairs in Sherbrooke, Canada

Cited by 72 publications

References 31 publications

Heterogeneous Contribution of Insulin Sensitivity and Secretion Defects to Gestational Diabetes Mellitus

Heterogeneous Contribution of Insulin Sensitivity and Secretion Defects to Gestational Diabetes Mellitus

Validation of a DNA methylation reference panel for the estimation of nucleated cells types in cord blood

Associations of Maternal Leptin with Neonatal Adiposity Differ according to Pregravid Weight

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