Gestational diabetes mellitus (GDM) is a growing threat to pregnancies, affecting both short- and long-term health of mother and child. GDM may be diet-controlled or require pharmacological intervention; causes of more severe GDM remain unclear. The placenta has a critical role in maternal insulin resistance and stress response. Therefore, it may play a part in GDM management. This study aimed to investigate placental antioxidant function in GDM, specifically, whether there is a distinction between diet- and medication-treated GDM pregnancies, and if such changes are reflected in maternal sera.

Placentae were grouped as: control (no complications), diet-controlled GDM (GDMD), and medicated GDM (GDMM). Groups were matched for maternal age, BMI, gestational age, and infant weight, and grouped by infant sex (n=8 per group). Maternal sera were grouped into control (n=8) and GDM (n=8), and similarly matched. For the placentae, both cytosolic and mitochondrially-enriched fractions were extracted. Total antioxidant capacity (TAC) was measured in placentae and sera, catalase (CAT) activity was measured in placentae, thioredoxin Reductase (TRxR) activity was measured in placentae, glutathione peroxidase (GPX) activity was measured in placentae, total cyclooxygenase (Total COX) and cyclooxygenase-2 (COX-2) activity was measured in placentae, heme oxygenase (HeOx) levels were measured in placentae, and selenoproteins (SELS) levels were measured in placentae.

The study found that placental TAC and the function of specific antioxidant systems were affected by GDM and fetal sex. Cyclooxygenase activity was increased in GDM pregnancies with male foetuses. Placental HeOx, but not SELS protein levels, was decreased in GDM. SELS protein was confirmed in human placental protein. These results suggest that TRxR may have a significant role in the redox regulation of GDM, further that increased COX activity may be characteristic of non-medicated GDM, and that SELS protein is present in human placenta.