ArticleScientific reports2026
Maternal and cord-blood inflammatory markers and BDNF in diabetic vs. non-diabetic pregnancies.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Maternal diabetes is associated with increased systemic inflammation and has been linked to adverse neonatal outcomes, including developmental delays that persist into early childhood. In this study we sought to characterize and compare the maternal levels and fetal cord-blood levels of the inflammatory markers C-reactive protein (CRP) and IL-6, as well as the neurotrophin brain-derived neurotrophic factor (BDNF) between mothers with pre-gestational Type-1 diabetes (T1DM) or Type-2 diabetes (T2DM), and non-diabetic controls (nonDM).A prospective cohort design was employed, analyzing biomarker concentrations during the third trimester in 98 pregnant women ages 18-40 years of age including 16 participants with T1DM, 49 participants with T2DM and 33 control participants matched for gestational age and body mass index (BMI) to control for confounding factors such as obesity. Plasma samples were collected at 28-30 weeks, 34-36 weeks, delivery, and from cord blood. The biomarkers CRP, IL-6, and BDNF were measured using standardized assays, and concentrations were compared among groups using ANOVA.In T2DM mothers, CRP levels were 2x higher in the third trimester as compared to nonDM controls. In T1DM mothers, IL6 levels were 3x lower than nonDM controls and 3.4x lower than T2DM. While not reaching statistical significance, cord-blood levels of IL6 were higher in T2DMs than other groups (p = 0.052). When examining BDNF levels, no differences were observed between groups.This study emphasizes the importance of addressing inflammation-related risks in pregnancies affected by diabetes. Targeted interventions may mitigate adverse neonatal outcomes and improve health trajectories. Future research should explore direct pathways linking maternal inflammation to fetal neural function to inform clinical strategies.
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