Intrauterine growth restriction is a major cause of perinatal mortality and morbidity. Injection of an adenovirus (Ad) vector containing the vascular endothelial growth factor-A165 (VEGF-A165) gene into the uterine arteries increased growth velocity and birth weight (trend) in growth restricted fetal sheep (1,2). Ad.VEGF-A165 treatment increased mRNA levels of the VEGF receptor FLT1/KDR in maternal but not fetal placental tissues and placental efficiency near term (trend) (1,2). We measured late gestation placental expression of genes regulating growth (insulin-like growth factor receptor 1, IGF-1R), lipid handling (lipoprotein lipase, LPL) and amino acid transport (TAT1) in normal and growth-restricted pregnancies with and without Ad.VEGF-A165 treatment. Single embryos (from superovulated single sire inseminated donor ewes) were transferred into adolescent recipient ewe uteri under general inhalational anaesthesia (isoflurane in O2/NO). Recipients were fed control (C n=12) or high (H n=45) intake of complete diet from 4-131 days’ gestational age (dGA term=145dGA) to induce normal and restricted fetal growth, respectively (3). At 89dGA under general anaesthesia (induction with propofol IV then as above) both uterine arteries were injected with 5×1011 particles of Ad.VEGF-A165 (H-Ad.VEGF, n=18) or control vector Ad.LacZ/control saline (H-Ad.LacZ/saline, n=27; C-saline, n=12). At 131dGA ewes were killed (pentobarbitone overdose IV). RNA was extracted from separated fetal and maternal placental compartments (frozen at -80C) and real-time quantitative PCR was performed to measure mRNA levels of LPL, TAT1 and IGFR-1 (normalised to GAPDH and βactin geometric mean). Data are mean±SEM and were analysed by two-way ANOVA (placental compartment and group [C-saline; H-Ad.VEGF; H-Ad.LacZ/saline]) then Least Squares Difference correction. Regardless of placental side TAT1 and LPL mRNA levels were lower in H-Ad.VEGF compared to H-Ad.LacZ/saline (TAT1, 0.54±0.08 vs. 0.75±0.06, P=0.02; LPL, 0.77±0.09 vs. 0.97±0.07, P=0.06) and compared to C-saline (TAT1, 0.54±0.08 vs. 0.76±0.09, P=0.07; LPL, 0.77±0.09 vs. 1.03±0.10, P=0.06). Regardless of group LPL, IGFR-1 and TAT1 mRNA levels were greater in the fetal compared to maternal placental side (LPL: 1.22±0.07 vs. 0.66±0.07; IGFR-1: 1.19±0.07 vs. 0.99±0.07; TAT1: 1.24±0.07 vs. 0.13±0.06; P <0.05). These data suggest that increased fetal growth velocity following Ad.VEGF-A165 is independent of altered IGFR-1 gene expression. Decreased TAT1 and LPL gene expression following Ad.VEGF-A165 is unexpected but may reflect complex amino acid and lipid transport regulation in these animals which requires further molecular analysis. Higher expression of genes related to nutrient transfer in the fetal-facing placental portion may indicate membrane specific placental nutrient transport mechanisms.