• Fetal programming of impaired decidualization in the offspring of diabetic rats.

GATTI CINTIA, SABRINA ROBERTI, MARÍA LAURA LEONARDI, ROMINA HIGA, ALICIA JAWERBAUM.

Congreso; IADPSG 2022 Meeting - International Association of the Diabetes and Pregnancy Study Groups Meeting 2022.; 2022

INTRODUCTION: Diabetes mellitus is a metabolic pathology that leads to placental, fetal and offspring’s alterations. Little is known regarding putative alterations in the uteri of the offspring of diabetic mothers. Peroxisome proliferator activated receptors (PPARs) are nuclear receptors involved in metabolic, anti-inflammatory and developmental pathways. PPARs regulate the expression of prolactin, insulin like growth factor binding protein 1 (IGFBP1) and fatty acid bindingprotein 4 (FABP4), endocrine mediators of decidualization. AIM: To address decidualization by evaluating the expression of genes codifying for PPARalpha, PPARgamma, prolactinand IGFBP1 and the protein levels of prolactin and FABP4 in the decidualized uteri of prepubertal offspring of diabetic and control rats. METHODS: A mild pregestational diabetic rat model was induced in F0 females by neonatal administration of streptozotocin (90 mg/kg sc). Control and diabetic females were mated with healthy males. The uteri of the female offspring (F1) were evaluated on postnatal day 30, after induction of decidualization with PMSG (50 UI) and hCG (50UI). In the decidualized uteri, Ppara, Pparg, Prl1 and Igfbp1 mRNA levels were evaluated by RT-qPCR and prolactin and FABP4 levels were evaluated by Western blot.RESULTS: The offspring of diabetic rats showed an increase in Ppara mRNA levels compared to controls (0.84 foldchange, p