We tested the hypothesis that maternal consumption of dietary fat, independent from obesity, increases serum leptin in neonatal pups and predisposes them to adult obesity. Female rats were fed either high fat diet (HF), low fat diet (LF), or were fed the HF diet but pair-fed (PF) to the caloric intake of the LF group for 4 weeks prior to breeding and throughout gestation and lactation. Dams consuming the HF diet had increased adiposity and were hyperphagic. At weaning, pups born to obese dams had significantly higher body fat, serum leptin levels, and reduced insulin tolerance as compared to offspring of LF-fed dams. Pups were weaned onto a chow diet until 8 weeks of age when offspring were then fed either a HF or LF. At 18 weeks of age, offspring from obese HF dams weighed more than offspring from non-obese LF or PF dams and offspring eating a HF diet weighed significantly more than those eating a LF diet. Consequently, HF-fed offspring of obese HF dams weighed the most and LF-fed offspring from obese HF dams were similar in weight to HF-fed offspring from non-obese LF dams. These data suggest that maternal obesity exerts an independent effect on offspring body weight that is of similar magnitude as the effect of the offspring's adult diet. Furthermore, there was no difference in body weight between the non-obese LF and PF offspring on either diet. Taken together, these data suggest maternal adiposity, and not dietary fat per se, induces hyperleptinemia and insulin resistance in offspring, as well as an increased body weight that persists into adulthood.