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Maternal-fetal adipokine remodeling in obesity-complicated pregnancies: associations with neonatal macrosomia and NICU requirement

Sep 2026 · Frontiers in Endocrinology · Vol 17 · 0 citations · 38 references
Medicine

Abstract

Introduction Maternal obesity is associated with altered maternal–fetal adipokine profiles and adverse early neonatal outcomes. This study aimed to characterize maternal and fetal adipokine patterns across obesity severity groups and to evaluate their associations with macrosomia and neonatal intensive care unit (NICU) requirement. Methods In this prospective study, 126 singleton pregnancies were stratified into normal-weight, class I obesity, and class II–III obesity groups (n=42 each). Maternal venous and fetal cord blood adiponectin, leptin, asprosin, fetuin-A, retinol-binding protein-4 (RBP-4), adipsin, and glucose transporter-1 (GLUT-1) were assessed at delivery. Macrosomia and NICU requirement were evaluated using group comparisons, receiver operating characteristic (ROC) analyses, and multivariable logistic regression models. Results Maternal and fetal adipokine profiles differed significantly across obesity severity groups. Maternal fetuin-A, RBP-4, and adipsin levels, along with fetal leptin, fetuin-A, RBP-4, adipsin, and GLUT-1 levels, increased significantly with increasing obesity severity. In ROC analyses, fetal adipsin showed the highest discrimination for macrosomia (AUC=0.951), whereas fetal RBP-4 showed the highest discrimination for NICU requirement (AUC=0.781). In exploratory adjusted analyses, fetal adipsin remained associated with macrosomia (adjusted OR=5.43, 95% CI 2.14–13.77), whereas fetal RBP-4 remained statistically associated with NICU requirement (adjusted OR=3.31, 95% CI 1.87–5.86). Discussion Maternal obesity is accompanied by distinct maternal and fetal adipokine remodeling at delivery, with fetal adipsin and RBP-4 showing outcome-specific associations with neonatal macrosomia and NICU requirement, respectively. The compartment-specific biomarker patterns further suggest that the fetal metabolic response to increasing maternal adiposity is not simply a reflection of maternal circulating profiles. These exploratory findings warrant validation in larger, independent cohorts.

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