In developed societies, diets high in sugar & fat (HSHF) are commonly eaten by women of reproductive age & contribute to the increasing rates of maternal obesity & excessive weight gain during pregnancy. In mice, offspring of mothers fed an obesogenic HSHF diet during pregnancy develop cardiovascular & metabolic dysfunction as adults, even when their birthweight was normal [1]. However, little is known about the mechanisms operating in utero which might account for the detrimental postnatal effects. This study tested the hypothesis that an obesogenic diet alters growth & function of the placenta, responsible for nutrient transfer to the fetus. We examined the effect of feeding pregnant mice an obesogenic HSHF diet on placental growth & nutrient transport in relation to fetal growth & placental expression of imprinted genes & signalling pathways known to regulate growth & metabolism. Methods: C57BL6 female mice were fed a control diet (11%fat, 3%sugar) or an obesogenic HSHF diet (30%fat, 36%sugar) during pregnancy. On day (D) 16 or 19, placental transport of 14C-methyl aminoisobutyric acid (MeAIB) & 3H-methyl D-glucose (MeG) was measured in vivo. Placental expression of Slc38a1, Slc38a2, Slc38a4, Slc2a1, Slc2a3, Igf2, H19, Dlk1, Igf2r, Zac1, Snrpn, Grb10, Phlda2, Gtl2, Peg11, Peg3, Cdkn1c genes was quantified by Real Time PCR. Expression of proteins involved in phosphoinositol 3-kinase (PI3K) & mitogen activated protein kinase (MAPK) signalling was determined by Western blotting. Dietary differences were determined by ANOVA & linear mixed model repeated measures as required & significant if P<0.05. Results: HSHF diet reduced fetal weight in parallel with placental weight at D16 (P<0.001, Table). By D19, placental weight remained less in HSHF dams (P<0.001), whereas the weight of fetuses had normalised (Table). This change in fetal growth trajectory was associated with enhanced placental glucose & amino acid transfer & upregulated Slc2a3 & Slc38a2 nutrient transporter genes on D16 (Fig 1&2, P<0.03). In the HSHF placenta there was also increased expression of imprinted genes on D16 (Igf2, Dlk1, Snrpn, Grb10 & H19, P<0.005, Fig 2) & PI3K & MAPK signalling proteins on D16 & D19 (PI3K p110α, pAkt, pGsk3 & pMAPK, P<0.04). Conclusion: Placental transport adapts to an obesogenic HSHF diet through local changes in signalling pathways & imprinted genes involved in growth & metabolism. These adaptations help meet the fetal drive for growth even though placental growth is compromised by a HSHF diet. However by altering the provision of specific nutrients, dietary-induced changes in placental phenotype have an important role in tissue programming with implications for the adult health of infants of women eating obesogenic diets