Pregestational Body Mass Index Is Associated with Differential Expression of ABC Transporter in the Maternal-Neonatal...

Background: Maternal obesity has been associated with fetal growth abnormalities and alterations in metabolic programming. ATP-binding cassette transporters, including ABCA1, ABCG1, ABCC1 and ABCG2, play essential roles in cholesterol homeostasis and placental function, fetal growth and development. However, the regulation of these transporters in the maternal-fetal axis under metabolic stress remains poorly understood. Methods: We evaluated 92 mother-newborn pairs, stratified by pregestational body mass index into three groups: normal weight (n = 34), overweight (n = 35) and obese (n = 23). Metabolic profiles and ABCA1, ABCG1, ABCC1 and ABCG2 mRNA expression in peripheral blood mononuclear cells were assessed. Results: Obese mothers demonstrated significantly higher TyG-BMI indices compared to normal-weight women. Regarding transporter expression, ABCA1 levels were elevated, while ABCG1 and ABCG2 were significantly downregulated in both overweight and obese mothers and their newborns. Positive correlations were observed between maternal and neonatal ABCA1. Maternal metabolic status correlated with ABC transporter expression, as demonstrated by inverse relationships between fasting glucose and maternal ABCA1 expression and between cholesterol levels and maternal ABCG2 expression. Furthermore, ABCG1 and ABCG2 expression levels positively correlated with fetal growth parameters. Conclusions: Maternal overweight and obesity before pregnancy were associated with significant changes in the expression of key ABC transporters in both mothers and their newborns. Changes in maternal ABCA1 and ABCG1 expression could be related to altered cholesterol homeostasis, while reduced ABCG2 expression possibly reflects changes in pathways involved in cellular protection and the handling of potentially harmful compounds. Further longitudinal studies are required to clarify underlying mechanisms and determine their persistence postnatally.