Poor intrauterine conditions perturb fetal development and predispose offspring to adult disease. A common cause of this is maternal undernutrition, which impairs fetal nutrient supply. The placenta is a critical determinant of fetal nutrient supply and adequate placental nutrient transfer relies on the development of a complex vascular network. Therefore, undernutrition may compromise fetal development by disrupting placental vascular development. This study aimed to examine the effects of maternal protein restriction on fetal growth and placental vascularity in C57BL/6J mice. Dams consumed a control (20% casein) or low-protein (8.7% casein) diet during pregnancy. At E18, fetal growth was assessed using weight and morphometric measures. Microfil was used to create casts of the feto-placental arterial vasculature. Micro-computed tomography-generated images were analysed to determine the total volume, length, and number of segments in these vascular networks. Placental expression of the angiogenic factors vascular endothelial growth factor A (Vegfa), angiopoietin 1 (Angpt1), and angiopoietin 2 (Angpt2) were measured using real-time qRT-PCR. Protein restriction significantly reduced female fetal weight but not male weight. Decreased female weight was accompanied by increased Angpt2 expression in the labyrinth zone of the placenta. However, there were no changes in morphology of the placental vascular casts. The female-specific changes in fetal growth and placental gene expression observed in this study contribute to a growing body of evidence that the female conceptus is more responsive to mild gestational stressors compared to the male. While there were no changes in the measures of placental vascularity in this study, it is possible that changes at the capillary level of the vasculature (which is currently under investigation) may contribute to the observed decrease in female fetal growth. This is as disproportional increase in Angpt2 is known to associate with capillary regression.