Human epidemiological and animal studies show that maternal nutrient reduction (MNR) and maternal overnutrition/obesity (MO) alter fetal growth and development, predisposing offspring (F1) to endocrine and appetite dysregulation. Compared to F1 of control-fed ewes, F1 of MO ewes display hypercortisolemia at birth and fail to exhibit the neonatal leptin surge implicated in lifelong appetite regulation. Here, we determined if MNR also elevates newborn lamb plasma cortisol and eliminates the neonatal leptin surge. Starting 30 d prior to conception, nulliparous control (CON, n = 6) ewes ate 100% NRC recommendations through parturition. Nutrient-reduced (NR, n = 6) ewes ate a CON diet through day 27 of gestation. From gestational days 28 to 78, NR ewes ate 50% of the CON diet before realimentation to 100% NRC recommendations. Jugular blood was collected daily from lambs from birth (day 0) through postnatal day 10, to determine plasma cortisol and leptin. Newborn NR plasma cortisol concentrations were increased (P < 0.0001) vs. CON and were similar to concentrations in MO lambs. Plasma leptin concentrations were similar between groups through postnatal day 7. The leptin surge, seen in CON lambs on postnatal days 8 to 10 was not present in NR lambs. These data show that, similar to MO lambs, early pregnancy MNR elevates newborn lamb plasma cortisol and eliminates the neonatal leptin surge. In the light of the similar elevation of neonatal cortisol in MNR and MO lambs, we conclude that cortisol plays a central role in regulating the neonatal lamb leptin surge.