This chapter reviews the maternal obesity literature, which suggests that epigenetic modulation of gene expression is likely to serve as one of the more promiscuous molecular mechanisms with which these maternal and early developmental footprints are cast. A study of epigenetic modifications in the development of obesity is a new and burgeoning field. Using animal models of maternal obesity, changes in fetal phenotype are being characterized. Prader-Willi syndrome is an imprinting disorder, which yields striking evidence for epigenetic mechanisms in the etiology of obesity. Experiments with mice containing the A vy allele have shown direct evidence of alterations in maternal diet leading to increased body weight of the offspring, concomitant with methylation changes in the fetal Agouti promoter. The chapter argues that in accordance with the developmental origins of adult disease hypothesis, perturbations in the in utero environment influence the development of diseases later in life.