The Impact of In Utero Exposure to Diabetes on Childhood Body Mass Index Growth Trajectories: The EPOCH Study

Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver, Aurora, CO, USA.
The Journal of pediatrics (Impact Factor: 3.79). 06/2011; 158(6):941-6. DOI: 10.1016/j.jpeds.2010.12.007
Source: PubMed


To examine associations between exposure to maternal diabetes in utero and body mass index (BMI) growth trajectories from birth through 13 years of age among a diverse cohort of youth.
Mixed linear effects models were constructed to assess differences in BMI and BMI growth velocity from birth through 13 years of age for 95 subjects exposed to diabetes in utero and 409 unexposed subjects enrolled in a retrospective cohort study.
The overall BMI growth trajectory (adjusted for sex and race/ethnicity) was not significantly different for exposed and unexposed subjects from birth through 26 months of age (P = .48). However, the overall growth trajectory from 27 months of age through 13 years differed by exposure status (P = .008), adjusted for sex and race/ethnicity. The difference was primarily due to a significantly higher BMI growth velocity among exposed youth between 10 and 13 years, increasing by 4.56 kg/m² compared with 3.51 kg/m² in the unexposed (P = .005). Control for demographic variables, socioeconomic factors, and maternal prepregnancy BMI did not alter the observed associations.
Exposure to maternal diabetes in utero accelerates BMI growth in late childhood, thus increasing long-term obesity risk.

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    • "Maternal obesity and gestational diabetes mellitus (GDM) create an intrauterine environment that promotes fetal overgrowth (Group HSCR, 2008; Catalano et al. 2009), altered body composition (Catalano et al. 2009; Uebel et al. 2014), and increased risk of childhood obesity (Crume et al. 2011). As the interface between maternal and fetal circulations, the placenta represents a vital determinant of fetal growth through its role in nutrient delivery to the fetus. "
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    • "So far it has been unclear at what age the effect prenatal environment starts to influence offspring weight gain. In a recent work diabetes exposure in utero started to show after 27 months of age in offspring BMI development [17], and in the HAPO study there was no difference in offspring weight regarding maternal glucose level during pregnancy at the age of two years despite the significant effect of maternal glucose level on birthweight [7,18]. In several studies prepubertal offspring of mothers with GDM or maternal excess weight gain during pregnancy had a greater risk for overweight and adiposity [14,19-21]. "
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    ABSTRACT: Environmental contributions to the development of childhood obesity may include a suboptimal in utero environment, diabetes and/or obesity in pregnancy, and pre- and postnatal exposure to environmental chemicals, also known as obesogens. Epigenetic modifications may be one mechanism by which exposure to an altered intrauterine milieu or metabolic perturbation may influence the phenotype of the organism much later in life. Epigenetic modifications of the genome provide a mechanism that allows the stable propagation of gene expression from one generation of cells to the next. This chapter highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin remodeling and histone modifications play key roles in adipogenesis and the development of obesity. Epigenetic modifications affecting processes important to glucose regulation and insulin secretion have been described in the pancreatic β-cells and muscle of the intrauterine growth retarded (IUGR) offspring, characteristics essential to the pathophysiology of type 2 diabetes (T2DM). Epigenetic regulation of gene expression contributes to both adipocyte determination and differentiation in in vitro models. The contributions of histone acetylation, histone methylation, and DNA methylation to the process of adipogenesis in vivo remain to be evaluated. KeywordsObesity-Epigenetics-Fetal growth-Diabetes
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