Developmental programming can be defined as a stimulus during a critical period, when the system is still plastic and may show susceptibility to environmental effects. Neonatal nutrition may modify circulating leptin levels, leading to changes in the maturation of hypothalamic circuitry, causing modifications of feeding behavior in adult life. Using the manipulation of litter size as a model of programming we aimed to investigate in male Wistar rats body weight gain, food intake profile, white adipose tissue (WAT) mass, plasma leptin levels and STAT-3 expression in the hypothalamus in adult life. After birth litters were adjusted as follows: small (3 pups-SL), normal (10 pups-NL) and large (16 pups-LL). Body weight gain was measured every week and food intake was determined between 50th to 60th day. At the 60th day rats were decapitated, trunk blood was collected for Elisa assay, retroperitoneal and epididymal WAT were weighed and the hypothalamus was dissected for Western blotting assay. Experimental procedures were approved by the ethics committee (protocol 060/2011). Data were analyzed using one-way ANOVA, followed by Dunnett’s post-test, using NL group as control. Difference was set at p<0.05 (n=8-16). SL rats had a higher body weight, while LL rats reached the same body weight as NL ones at 60th day (NL:408.5+8.5g; SL:476.5+14.9g; LL:381.8+8.4g). LL rats had an increase in food intake (NL:82.3+1.6g/100g bw; SL:82.8+2.7g bw; LL:97.2+2.0g bw). Both groups, SL and LL, had higher contents of WAT compared to NL (NL:6.65±0.47g; SL:12.48±0.85g; LL:9.21±0.52g). SL rats showed significant hyperleptinaemia in adult life, with no difference in the LL rats, compared to NL (NL:4.0±0.3ng/mL; SL: 5.9 ± 0.7 ng/mL; LL: 4.8 ± 0.4 mg/mL). p-STAT-3 expression in the hypothalamus was decreased in SL and LL rats, compared to NL. Our data suggest that changes in food availability during neonatal life may underlie long lasting effects in energy homeostasis in adult life, with impact on body weight, food consumption, plasma leptin and central leptin signaling, which ultimately may contribute to overweight and obesity.