Placental research is increasingly focused on how the organ adapts to support adequate fetal growth in a potentially sub-optimal nutritional environment. However, the precise mechanisms by which specific micronutrients, such as zinc, contribute to pregnancy success remain unknown. Evidence suggests an association between maternal zinc deficiency and the development of placental-related pregnancy complications such as preeclampsia and intrauterine growth restriction. We used a dietary deficient mouse model to determine the effects of zinc deficiency on placental and fetal development and pregnancy outcome. Seven week old C57Bl6 females were fed either a control (40 mg/kg zinc) or zinc deficient (10 mg/kg) diet (n=30 per group) for 6 weeks prior to mating and throughout pregnancy. A small subset of animals was selected to undergo radio-telemetry surgery to continuously measure blood pressure throughout pregnancy and lactation. The remaining females were mated and at day 18.5 of gestation, pregnant dams were sacrificed and placentas and fetuses weighed and collected for histological and molecular analyses. Average 24-hour mean arterial pressure was significantly elevated in the zinc deficient mice prior to pregnancy (p<0.01) and continued to increase throughout pregnancy and lactation (p<0.01 for both). Marginal zinc deficiency prior to and during pregnancy resulted in a 7% decrease in fetal weight (p<0.01) and pups were significantly smaller 3 days after birth until weaning (12% lighter and 33% lighter; respectively, both p<0.01). The decreased fetal weight was accompanied by a 10% reduction in placental weight at day 18.5 of gestation (p<0.01). However, structural analysis of the zinc deficient placentas revealed no significant differences in the mid-sagittal cross-sectional areas of the junctional and labyrinth zones despite a significant 12.5% reduction in labyrinth weight (p<0.05). These indicate potential compensatory mechanisms that render the zinc deficient placenta structurally similar but smaller than controls but remain insufficient to maintain fetal growth.