Comparative analysis of inflammatory and metabolic biomarkers in PGDM and GDM pregnancies

Pregestational diabetes mellitus (PGDM) and gestational diabetes mellitus (GDM) are associated with adverse pregnancy outcomes through inflammatory and metabolic dysregulation. This study compared serum levels of pro-early placental insulin-like growth factor (pro-EPIL), galectin-3, sirtuin-1 (SIRT-1), matrix metalloproteinase-10 (MMP-10), chemerin, and interleukin-33 (IL-33) in diabetic pregnancies and explored their inter-correlations. This cross-sectional study included pregnant women at 24–39 weeks of gestation, categorized into normal glucose tolerance (NGT, n = 30), PGDM (n = 17), and GDM (n = 33) groups. Serum biomarker concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Pro-EPIL and galectin-3 were significantly elevated in PGDM compared to NGT (p < 0.05), while GDM showed no significant difference from either group. Both PGDM and GDM demonstrated significantly higher MMP-10, chemerin, and IL-33 levels compared to NGT (p < 0.05). SIRT-1 concentrations did not differ significantly among groups. Correlation analysis revealed that SIRT-1 was positively correlated with chemerin and IL-33 across all groups, with progressively stronger associations in GDM (r = 0.669 and r = 0.811, respectively; p < 0.01). MMP-10 showed significant positive correlations with IL-33 in all groups, strongest in GDM (r = 0.648, p < 0.01). Galectin-3 exhibited significant correlations with SIRT-1 and MMP-10 exclusively in the GDM group. PGDM and GDM exhibit distinct and overlapping biomarker profiles reflecting inflammatory and metabolic processes. Pro-EPIL and galectin-3 elevation specifically in PGDM suggests prolonged metabolic stress, while increased MMP-10, chemerin, and IL-33 in both conditions indicate shared inflammatory pathways. The correlation analysis identified SIRT-1, MMP-10, and IL-33 as an interconnected network with progressively stronger associations in GDM, while GDM-specific galectin-3 correlations suggest presence of unique pathogenetic mechanisms.