Akademik Veri Yönetim Sistemi
International Journal of Gynecology and Obstetrics, 2025 (SCI-Expanded, Scopus)
Objective: Gestational diabetes mellitus (GDM) is a hyperglycemic condition that develops during pregnancy and poses significant risks to maternal and fetal health. Oxidative stress plays a crucial role in the pathogenesis of GDM by disrupting insulin signaling pathways and contributing to β-cell dysfunction. Carbonic anhydrase (CA) enzymes, particularly CA-I and CA-II, are involved in pH regulation and metabolic homeostasis. However, the relationship between oxidative stress and CA enzyme activity in GDM remains unclear. The aim of the present study was to evaluate CA-I and CA-II levels and their association with oxidative stress parameters in GDM patients. Methods: This case–control study included 30 pregnant women with GDM and 30 healthy pregnant controls. Baseline characteristics were fully reported; differences between groups were examined using covariate-adjusted analyses. Serum levels of CA-I, CA-II, malondialdehyde (MDA), total oxidant status (TOS), and total antioxidant capacity (TAC) were measured using enzyme-linked immunosorbent assay (ELISA) kits. Statistical analysis was performed using SPSS 25, with significance set at P < 0.05. Results: CA-I and CA-II levels were significantly higher in the GDM group compared to control (P < 0.05). MDA and TOS levels were also elevated in GDM patients, indicating increased oxidative stress, whereas TAC levels were significantly lower (P < 0.05). Receiver operating characteristic (ROC) analysis revealed that CA-I, CA-II, MDA, and TOS exhibited strong discriminatory power in differentiating GDM patients from healthy controls. In a multivariable linear regression adjusting for age, body mass index (BMI), gestational age at sampling, and parity, GDM was associated with higher CA-I (β = 3.1, 95% confidence interval [CI]: 1.6–4.6) and CA-II (β = 2.4, 1.1–3.7), higher MDA (β = 0.27 per 0.1-unit) and TOS (β = 4.1 per unit), and lower TAC (β = −0.22 per 0.1-unit; all P ≤ 0.004). In logistic regression, CA-I, CA-II, MDA, and TOS independently increased the odds of GDM, while TAC was inversely associated (adjusted odds ratios [ORs] 1.28, 1.17, 1.15, 1.05, and 0.87, respectively), with excellent model performance (area under the curve [AUC] 0.86; Hosmer–Lemeshow P = 0.67). Conclusion: Increased CA-I and CA-II levels in GDM patients suggest a potential role for CA enzymes in the metabolic dysregulation associated with GDM. The strong correlation between oxidative stress markers and CA enzyme activity highlights their potential as diagnostic and prognostic biomarkers for GDM. Future studies should explore the mechanistic pathways linking CA enzymes with oxidative stress and insulin resistance to identify novel therapeutic targets.