Perinatal risk factors for childhood obesity and metabolic dysregulation

Abstract

Background: Childhood obesity has increased significantly in recent decades. Objective: The objective was to examine the perinatal risk factors related to childhood obesity. Design: In a prospective study, 89 women with normal glucose tolerance (NGT) or gestational diabetes mellitus (GDM) and their offspring were evaluated at birth and at 8.8 6 1.8 y. At birth, obstetrical data, parental anthropometric measures, and neonatal body composition were assessed; at follow-up, diet and activity were assessed and laboratory studies were conducted. Weight was classified by using weight for age and sex, and body composition was measured by using dual-energy X-ray absorptiometry. In childhood, data were analyzed as tertiles and prediction models were developed by using logistic and stepwise regression. Results: No significant differences in Centers for Disease Control and Prevention weight percentiles, body composition, and most metabolic measures were observed between children of mothers with NGT and GDM at follow-up. Children in the upper tertile for weight had greater energy intake (P = 0.02), skinfold thickness (P = 0.0001), and leptin concentrations (P , 0.0001) than did those in tertiles 1 and 2. Children in the upper tertile for percentage body fat had greater waist circumference (P = 0.0001), insulin resistance (P = 0.002), and triglyceride (P = 0.009) and leptin (P = 0.0001) concentrations than did children in tertiles 1 and 2. The correlation between body fat at birth and follow-up was r = 0.29 (P = 0.02). The strongest perinatal predictor for a child in the upper tertile for weight was maternal pregravid body mass index (BMI; kg/m 2 ) .30 (odds ratio: 3.75; 95% CI: 1.39, 10.10; P = 0.009) and for percentage body fat was maternal pregravid BMI .30 (odds ratio: 5.45; 95% CI: 1.62, 18.41; P = 0.006). Conclusion: Maternal pregravid BMI, independent of maternal glucose status or birth weight, was the strongest predictor of childhood obesity.

Mitochondrial biogenesis is decreased in skeletal muscle of pig fetuses exposed to maternal high-energy diets

“…These diseases are due to multifactorial causes that include genetic and environmental factors (O'Rahilly et al, 2005). Human epidemiological and animal experimental studies indicate that alteration in fetal growth and development in response to prenatal environmental conditions such as nutritional stimulus may have deleterious persistent health effects lasting for the entire life (Wu et al, 2004;Catalano et al, 2009). Researches have demonstrated a link between maternal malnutrition and offspring risk of metabolic diseases (Barker et al, 1993;Tappia et al, 2013).…”

Leptin and adiponectin in the female life course

“…In fact, hyperleptinemia during neonatal life may program leptin resistance via dual effects on food intake and energy expenditure, with long-term adverse consequences for the hypothalamic circuits regulating energy balance (2,35). Some studies have shown an increased risk for obesity and insulin resistance in neonates born to obese mothers, as well as higher levels of leptin and markers of inflammation than in infants born to lean mothers (36).…”

Offspring DNA methylation of the aryl-hydrocarbon receptor repressor gene is associated with maternal BMI, gestational age, and birth weight

“…1 Risk factors for obesity start to accrue even in fetal life and include maternal obesity 2 and slow or fast fetal growth. 3 Preterm birth itself has been variably associated with later onset of metabolic disorders related to obesity such as insulin resistance and hypertension.…”