Experimental gestational diabetes mellitus (GDM) induced by intrauterine programming effects of F0 treatments with mitochondrial antioxidants.

I LINENBERG, V WHITE, A JAWERBAUM, E CAPOBIANCO.

CABA

Congreso; Scientific IADPSG Meeting 2016; 2016

In a mild model of diabetes induced by neonatal streptozotocin administration (F0), we have previously found that the female offspring, when mated with control males, develop GDM during pregnancy. Considering that an intrauterine pro-oxidant and pro-inflammatory environment is evident in both mild diabetic F0 pregnancies and GDM pregnancies, the AIM of this work was to address whether F0 maternal treatments with mitochondrial antioxidants reduce pro-oxidant and pro-inflammatory markers in GDM placentas (F1). METHODS: Control and mild diabetic (glycemia 180-220 mg/dl) Wistar rats (F0) were treated with either vehicle or antioxidants (Idebenone (IDE, 100 mg/kg/day) or Mitoquinone (MitoQ, 17mg/kg/day)) from day 1 of gestation until parturition. No treatments were performed in the F1 generation. The female offspring (F1) from control and diabetic rats were mated with healthy males. On day 21 of pregnancy, rats were euthanized, the serum conserved for metabolic determinations and the placentas preserved for evaluation of a) levels of PPARγ, superoxide dismutase (SOD) and nitrotyrosine (a marker of protein nitration and peroxynitrite-induced damage), by immunohistochemistry, b) the production of nitric oxide, through quantification of nitrates/nitrites by the Griess reaction and c) apoptosis, by TUNEL. RESULTS: The offspring of diabetic rats had increased glycemia and insulinemia (p