CONICET | Buscador de Institutos y Recursos Humanos

Fetal exposure to glucocorticoids excess has been implicated as a causative factor in fetal growth restriction. The objectives of the present study were: a) to develop a murine model of IUGR induced by prenatal exposure to dexamethasone, which mimics maternal stress, and b) to evaluate maternal, feto-placental and neonatal status. Pregnant BALB/c mice were treated with various daily doses of dexamethasone (2, 3, 5 and 8 mg/kg, s.c.) starting from gestational day 14 to 16. The control group was sham-treated with saline. Body weight gain and food intake of pregnant mice were monitored. Also, maternal corticosterone levels were determined 24 h before labor. On gestational day 16, 17 and 18 the placental and fetal weights were recorded. At postnatal day 1, crown:rump length, abdominal and head circumference, and the pups weight were measured. IUGR was diagnosed when the body weight of each fetus/pup was below the 10th percentile of body weight of the control group for each gestational age and for the postnatal day 1. Data were analyzed by one-way ANOVA and comparisons were made by Tukey?s test. The dose of 8 mg/kg/day of dexamethasone administered on days 14 and 15 of pregnancy greatly increased IUGR rate from 39% (spontaneous IUGR) to 87% at postnatal day 1 (p?0.05). Anthropometric measurements showed a symmetrical IUGR. Also, the average weight of the pups was 28% lower than control (p?0.05). On gestational days 16, 17 and 18, the decrease in fetal growth also became evident. On gestational day 18, glucocorticoid overexposure reduced fetal weight and placental mass by 12%. Dexamethasone exposure resulted in a significantly decreased maternal serum corticosterone levels (by 13%, p?0.05) and maternal body weight gain (by 48%, p?0.001) on gestational day 18. Collectively, our results suggest that short-term exposure to dexamethasone during late pregnancy adversely affects fetal and placental growth trajectory leading to IUGR.