In the past decade, epidemiological findings and data from experimental studies in animals have shown that the structure and function of the organism can be programmed during critical periods of development which can lead to detrimental long-term consequences for the health of an individual. Low birth weight has been linked to many adult diseases in humans including type 2 diabetes. The full detrimental effects of early growth restriction are often accompanied by the presence of obesity, which itself might be a manifestation of programmed appetite regulation in fetal and neonatal life. The understanding of interactions between leptin and insulin and their roles in glucose and body weight regulation provides clues towards mechanisms underlying altered appetite regulation and increased risk of type 2 diabetes in low birth weight individuals. Molecular mechanisms involved might include epigenetic alteration of the fetal genome in response to maternal nutrition.