Introduction Fetal glucose supply is a key determinant of growth in utero. Deficient or excess glucose availability is associated with fetal growth restriction and macrosomia, respectively. Glucocorticoid stress hormones influence blood glucose availability by antagonizing the action of insulin, in the non-pregnant animal. Furthermore, they reduce fetal growth and alter placental nutrient transporter expression [1]. This study aimed to determine whether maternal glucocorticoid treatment affects hepatic release and placental transport of glucose in the pregnant mouse in vivo. Methods All procedures were conducted in accordance with the Animals (Scientific Procedures) Act 1986. C57BL6/J mice (n=20) were treated with corticosterone (CORT, 76 µg/g/day in drinking water) between day (D) 11 and D16 of pregnancy (term = D21). This procedure is established to raise circulating corticosterone to stressed levels [1]. On D16 or D19, materno-fetal clearance of 3H-methyl-D-glucose (MeG) was measured under anaesthesia (fentanyl-fluanisone:midazolam in water, 1:1:2) [2] then the dam was euthanized and samples of maternal plasma, liver and placenta were collected. Expression of the insulin-insensitive Slc2a1 and Slc2a3 glucose transporter genes was determined in placentae by qPCR. Hepatic glycogen content was determined by enzymatic conversion to glucose using amyloglucosidase. Glucose and plasma insulin concentrations were analysed by automated glucometer and ELISA, respectively. Data were analysed separately at D16 and D19 by Student’s t test and significance determined at the level P<0.05. Results are mean±SEM. Results Compared to untreated (UT) controls (n=51), CORT reduced placental weight on D16 and fetal weight on both D16 and D19. Maternal plasma insulin concentration was higher in CORT treated than UT dams on D16 (UT, 1.1±0.3 ng/ml, n=7; CORT 40.1±5.3 ng/ml, n=7; P<0.05) but not D19 (UT, 2.6±1.2 ng/ml, n=12; CORT, 2.0±0.7 ng/ml, n=12; P>0.05). However, neither hepatic glycogen content nor blood glucose concentration differed between UT and CORT dams at either gestational age (P>0.05). On D16, CORT increased placental expression of Slc2a1 and Slc2a3 (n=6 per group) but did not affect materno-fetal MeG clearance (UT, n=64 fetuses; CORT, n=25 fetuses) (Figure). Contrastingly, although placental Slc2 expression no longer differed from UT animals at D19, materno-fetal MeG clearance was increased by 26% in CORT treated dams (UT, n=41 fetuses; CORT, n=22 fetuses) (Figure). Discussion When maternal glucocorticoid concentrations are raised through stress, illness or exogenous administration, fetal glucose supply may be increased due to changes in placental transport, even if maternal metabolism is unaffected. Ultimately, this may alter fetal growth trajectory and increase neonatal morbidity and metabolic disease risk in the offspring.