Maternal obesity has dramatically increased in recent decades. The prevalence of pediatric neurodevelopmental disorders has also risen. As the perinatal environment influences the risk of these disorders, we hypothesize that exposure to maternal obesity impacts the development of neural circuits critical in behavioral regulation and thus alters offspring behavior. Moreover, we postulate that exposure to high-diet during perinatal development will impact the neuroendocrine system. A non-human primate model was used to examine the consequences of maternal obesity and high-fat diet (HFD) consumption on the behavior and stress response of adult females and their offspring. Female Japanese macaques consumed either a low fat diet (CTR; 13% of calories from fat) or a HFD (36% calories from fat) for two years prior to gestation. The mother and infant were examined on post-natal days (PND) 1, 7, 21 and 60. Social behavior was examined in the offspring in response to introduction to a novel peer at 6 months of age and with familiar peers in their home cage at 10 months of age. Cortisol was measured in the mothers prior to pregnancy and during the early third trimester and in the offspring at 4, 11 and 13 months of age. HFD mother-infant pairs consistently spent more time nursing. HFD mothers groomed their infants less on PND 1 and showed decreased maternal care at PND 21 and 60. At PND 21 and 60, HFD infants showed a reduction in social play and decreased contact with other monkeys. Diminished social interaction was also evident at 6 and 10 months of age. HFD offspring display an increase in anxiety and increased hair and plasma cortisol at all time points. These findings indicate that maternal obesity initiates a fetal environment that may result in neural reprogramming and predisposes HFD offspring to pediatric neurodevelopmental disorders.