Maternal obesity and obesogenic diets in pregnancy are associated with adverse outcomes for the mother and child. The placenta interfaces the mother and fetus during pregnancy and controls nutrient and oxygen transfer via its transport and endocrine functions. Placental formation and function depend on mitochondria, the energy powerhouses within cells. This study aimed to determine the effect of maternal obesity on placental development and mitochondrial function. Female mice were fed a standard (11%kcal fat and 7%kcal sugars) or obesogenic diet (36%kcal fat and 30%kcal sugars) for 6 weeks prior to and during pregnancy. On gestational day 19, fetal and placental tissues were collected. A representative placenta from each sex per litter was fixed for morphological assessment or separated into transport labyrinth zone (Lz) and endocrine junctional zone (Jz) for mitochondrial analysis. Data were analysed by t-test or mixed linear model (obesity, sex). Maternal obesity did not affect litter size, however, it reduced fetal and placental weights (male: -10% and -23% and female: -14% and -30%, all p<0.0005). In placentae from obese dams, the volume of the Lz was reduced in both sexes (males: -22%, females: -20%, both p<0.05). Further, in male offspring only, there was a reduction in the volume of the Jz (-29%, p=0.02) and spongiotrophoblast (-31%, p=0.004). There were no effects of diet or sex on fatty acid oxidation, complex I and II-linked mitochondrial respiration. However, Jz from obese dams showed a 30% increase in complex II respiration (p=0.08). Mitochondrial coupling efficiency and electron transfer system capacity were unaltered in the Jz of obese animals. Work is underway to assess mitochondrial function in the Jz of female and the Lz of female and male offspring. Maternal obesity adversely affects the formation of the mouse placenta in a sex-specific manner while preserving mitochondrial function in the placental endocrine region.