Abstract

BackgroundMaternal obesity increases adult offspring risk for cardiovascular disease; however the role of offspring adiposity in mediating this association remains poorly characterized.ObjectiveTo investigate the associations of maternal pre-pregnant body mass index (maternal BMI) and gestational weight gain (GWG) with neonatal cardio-metabolic markers independent of fetal growth and neonatal adiposity.MethodsA total of 753 maternal-infant pairs from the Healthy Start study, a large multi-ethnic pre-birth observational cohort were used. Neonatal cardio-metabolic markers included cord blood glucose, insulin, glucose-to-insulin ratio (Glu/Ins), total and high-density lipoprotein cholesterol (HDL-c), triglycerides, free fatty acids and leptin. Maternal BMI was abstracted from medical records or self-reported. GWG was calculated as the difference between the first pre-pregnant weight and the last weight measurement before delivery. Neonatal adiposity (percent fat mass) was measured within 72 hours of delivery using whole body air displacement plethysmography.ResultsIn covariate adjusted models, maternal BMI was positively associated with cord blood insulin (p=0.01) and leptin (p<0.001) levels and inversely associated with cord blood HDL-c (p=0.05) and Glu/Ins (p=0.003). Adjustment for fetal growth or neonatal adiposity attenuated the effect of maternal BMI on neonatal insulin, rendering the association non-significant. However, maternal BMI remained associated with higher leptin (p<0.0011), lower HDL-c (p=0.02) and Glu/Ins (p=0.05), independent of neonatal adiposity. GWG was positively associated with neonatal insulin (p=0.02), glucose (p=0.03) and leptin levels (p<0.001) and negatively associated with Glu/Ins (p=0.006). After adjusting for neonatal adiposity, GWG remained associated with higher neonatal glucose (p=0.02) and leptin levels (p=0.02) and lower Glu/Ins (p=0.048).ConclusionsMaternal weight prior and/or during pregnancy is associated with neonatal cardio-metabolic makers including leptin, glucose, and HDL-c at delivery, independent of neonatal adiposity. Our results suggest that intrauterine exposure to maternal obesity influences metabolic processes beyond fetal growth and fat accretion.

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