The impact of maternal nutrient restriction during early-to-mid gestation, a period coinciding with early fetal brain development, on appetite regulation and energy balance in the offspring following juvenile obesity was examined. Pregnant sheep were either fed to fully meet their nutritional requirements throughout gestation or 50% of this amount between 30-80 days gestation. Following weaning, offspring were either made obese through exposure to a sedentary obesogenic environment or remained lean. Maternal nutrient restriction had no effect on birth weight or subsequent growth. At one week of age, only, gene expression for neuropeptide Y in the hypothalamus was reduced in nutrient restricted offspring. By 1 year of age, all obese animals had raised plasma leptin, non-esterified fatty acids and insulin, with the latter effect amplified in nutrient restricted offspring. Fasting plasma glucose, triglycerides and cortisol were unaffected by obesity. The entrained reduction in physical activity that led to obesity persisted when all animals were maintained within individual pens. Obese nutrient restricted offspring, however, exhibited reduced daily food intake and were, therefore, no longer in positive “energy balance”. This adaptation was accompanied by elevated hypothalamic gene expression for the melanocortin-4 and insulin receptors, AMP-activated kinase and acetyl CoA carboxylase α. In conclusion, nutrient restriction specifically targeted over the period of early fetal brain development, contributes to a profoundly different adaptation in energy balance following juvenile obesity. The extent to which this adaptive response may benefit the offspring or result in an exacerbated risk for type II diabetes remains to be established.