Ketosis is a physiological metabolic state, in which fat is the primary energy source (vs glucose), and can be induced through fasting or ketogenic diets (KDs). KDs are rich in lipids and low in carbohydrates, are popular, however, limited literature exists on their safety during pregnancy. Given the essential role of glycolysis in axonal growth dynamics, we hypothesized that KD might disrupt proper axonal guidance during embryonic development, leading to alterations in brain connectivity.Thus, we placed pregnant mice on either a KD or a control diet (CD), starting from gestational day 8.5. KD embryos at day 14.5 showed elongated cortico-thalamic axons and an ectopic growth cones penetrating into the non-permissive subventricular zone, suggesting brain wiring alterations. Female adult mice subjected to KD during embryonic development displayed diminished performance in the rotarod task, more grooming behavior, and an inability to distinguish between a novel and a familiar mouse. KD males scent-marked less and discriminated less between self and non-self odors, despite sniffing longer and at higher frequencies than controls. Finally, analyses of ultrasound vocalization revealed differences in syllable types, with gestational KD mice having increased call duration and amplitude during female-male interactions than controls.Our findings indicate that a gestational KD results in sex-specific motor coordination deficits, increased self-grooming and alterations in social behavior and communication. Notably, these phenotypic traits are consistent with several developmental disorder models linked to autistic spectrum disorders. Therefore, our findings have potential implications for understanding human etiology of neurodevelopmental disorders.