Intrauterine growth restriction (IUGR) is a risk factor for cardiovascular disease, type 2 diabetes mellitus, and obesity in adulthood. Several studies on diverse geographic and ethnic cohorts have provided evidence that being born small for gestational age (SGA) increases adult disease risk through various pathways of metabolic dysregulation. Unfavorable influences in the fetal environment may program metabolic homeostasis in later life affecting blood pressure, glucose tolerance and lipid regulation. Fetal restricted protein supply may impair the development of the kidney and reduce the nephron number, which is involved in blood pressure regulation. Moreover, children exposed to IUGR may exhibit postnatal rapid catch-up growth, altered body composition, increased visceral adiposity and low adiponectin levels which predispose to cardiovascular disease and type 2 diabetes mellitus in adulthood. Impairment in fetal pancreatic development and subsequent insulin signalling deficits due to IUGR may also be involved in the pathogenesis of these conditions. This review summarizes some of the hypotheses that have been put forward to explain the association between fetal growth restriction and subsequent metabolic dysregulation that may increase adult disease risk.