The metabolic and cardiovascular complications associated with reduced fetal growth have been identified in the past 10 years. These include cardiovascular disease and the insulin resistance syndrome, comprising dyslipidaemia and impaired glucose tolerance or type 2 diabetes, and they appear to result from the initial development of insulin resistance. Although the mechanism underlying the development of insulin resistance associated with reduced fetal growth remains unclear, there is some evidence that adipose tissue plays a key role. Over the past decade, several hypotheses have been proposed to explain this unexpected association. Each points to either a detrimental fetal environment, genetic susceptibility or an interaction between the two. Although yet to be confirmed, the hypothesis suggesting that the association could be the consequence of genetic-environmental interactions is at present the most attractive.