Epidemiologic studies suggest a relationship between low birth weight and adverse cardiovascular outcomes. Risk factors such as obesity, insulin resistance, diabetes mellitus, and hypertension—the cardiometabolic syndrome—are similarly affected. These observations are now supported by numerous animal studies. The mechanisms linking low birth weight and the cardiometabolic syndrome later in life appear to be multifactorial and involve alterations in the normal cellular and physiologic systems associated with growth in an unfavorable environment. Such “fetal programming,” an adaptation to a shortage of nutrients, may bring about maladaptation upon postnatal exposure to an abundance of nutrients. This review briefly summarizes the adaptive responses in various models used to induce an intrauterine growth restriction, and discusses insights into the mechanisms mediating the fetal programming of the cardiometabolic syndrome.