Alcohol consumption during pregnancy can cause adverse fetal and offspring outcomes. During pregnancy, long term moderate and high dose ethanol (EtOH) consumption significantly alters maternal endocrine status, altering the in-utero environment, potentially contributing to these adverse offspring outcomes1. However, the effects of alcohol exposure during the periconceptional period (PcEtOH) on maternal endocrine status is unknown. As 50% of women consume alcohol during this period, it is important to determine the impact of this may have on maternal HPA physiology.
Female Sprague-Dawley rats were treated with PCEtOH (12/5% v/v EtOH, liquid diet) from 4 days before conception (E-4), until embryonic day 4 (E4). Maternal plasma was collected during and following EtOH exposure, and maternal adrenal glands were collected at E05 and E15. Plasma Corticosterone levels and adrenal gene expression were assessed.
PcEtOH increased plasma corticosterone concentrations before pregnancy. At E5, key steroidogenic genes (mc2r, stAr, cyp21a1, cyp11b1 and 11bhsd2) were not affected by PcEtOH, however relative mRNA expression of aldosterone regulating genes, cyp11b2 and agtr1a were significantly increased. Interestingly, at E5 plasma corticosterone concentrations were reduced but aldosterone unaffected by the PCEtOH. At E15, relative gene expression of mc2r, stAr, cyp21a1, cyp11b1, 11bhsd2 and agtr1a was significantly increased in animals who were exposed to PCEtOH.
These results suggest that maternal adrenal physiology may be altered both during PcEtOH exposure and throughout pregnancy. A reduction in corticosterone levels during early pregnancy may have consequences for blastocyst development, implantation and viability, whereas the observed increase in mRNA expression of steroidogenic genes later in pregnancy may indicate the propensity for elevated corticosterone within PcEtOH exposed dams in late pregnancy2. This may potentially influence the final stages of fetal development and parturition and contribute to disease susceptibility of offspring.