During pregnancy, adaptations in the maternal brain support an increase in food intake to meet the energy demands for a developing fetus. Similarly, in lactation energy demands are increased due to the production of milk. Pregnancy represents a vulnerable life stage for increased weight gain, as over 75% of pregnant women surpass the optimal weight gain recommended by the Institute of Medicine, yet there is little understanding of the mechanism underlying the increased food intake in these reproductive states. Ghrelin, an orexigenic hormone, activates Agouti-related peptide neurons in the arcuate nucleus promoting rapid food intake. Here, we investigate whether increased ghrelin sensitivity contributes to pregnancy- and lactation-induced elevation of food intake. Female C57BL/6J mice were administered with either ghrelin (0.3mg/kg) or vehicle (saline) i.p. at 4 time points; virgin, day 8 and 15 of pregnancy and lactational day 10. Food was removed 5 hours before treatment and returned at the time of treatment. Food intake was measured over the following 2 hours. Expectedly, ghrelin stimulated food intake in virgin mice compared to controls (2way ANOVA p = 0.0202). Surprisingly throughout pregnancy there was no ghrelin-induced increase in food intake compared to controls. Ghrelin sensitivity was restored in lactation where ghrelin administration increased food intake compared to controls (Mann-Whitney p = 0.0223). Bodyweight gain over 24hrs after ghrelin administration followed the same pattern. Virgin and lactating mice treated with ghrelin had a larger increase in body weight relative to controls (Mann-Whitney p = 0.0081, p = 0.477), yet no body weight difference was observed in pregnancy. The results suggest during pregnancy ghrelin does contributed to increased food intake. During lactation, however, increased sensitivity to ghrelin maybe a key factor in supporting the hyperphagia required to meet the energy demands of milk production.