This chapter focuses on observations of mechanisms relevant to the major postnatal pathophysiologies associated with uteroplacental insufficiency-induced intrauterine growth retardation (uIUGR): altered glucose homeostasis; altered lipid homeostasis; and hypertension. Multiple postnatal diseases associated with aberrant lipid homeostasis threaten the IUGR infant. Uteroplacental insufficiency-induced IUGR affects expression and function of genes involved in energy and lipid homeostasis in skeletal muscle. The pancreatic ß-cell obviously plays a central role in glucose homeostasis. In general, with uIUGR insulin resistance has been observed in association with hyperinsulinemia in juvenile and young adult animals. In both the sheep and the rat, uIUGR decreases nephron number. Epigenetic programming occurs in a gene-, tissue-, and gender-specific manner in response to a stress such as uIUGR. Mammalian epigenetics is complex, and the impact of altering epigenetic determinants may not be obvious or immediate.