Developmental programming in the animal kingdom has been recognised for decades amongst animal breeders and from studies of natural disturbance of the maternal/fetal environment. However, associations between birth weight and susceptibility to adulthood disease described by Barker and colleagues led to a plethora of studies in experimental animals designed to determine whether modulation of the in utero and/or neonatal environment has lasting consequence for offspring cardiovascular and metabolic function in adulthood. The earliest models described how diabetes in rodent pregnancy or a maternal diet deficient in protein led to disorders of glucose homeostasis in the offspring. Those currently employed include studies in which the maternal diet has been manipulated, determination of the consequences of reduced blood flow to the uterus and investigations into the effects of maternal stress or behavioural disturbance. Rats, rabbits, mice, guinea pigs and sheep have been utilised. Review of the literature reveals remarkable diversity of protocols eg in the timing of the nutritional intervention and in the parameters of cardiovascular and metabolic function evaluated in the offspring. Even amongst studies of the same intervention and the same animal, protocols between laboratories vary. Whilst this has not facilitated assimilation of information or the drawing of definite conclusions, similarities are apparent which may indicate commonality of mechanism. Offspring of rodents subjected to maternal hyperglycaemia, maternal protein restriction, global reduction of maternal diet or maternal dietary fat supplementation share common disorders of glucose homeostasis. Offspring are frequently insulin resistant and show early anomalies of pancreatic function and structure. Adulthood insulin resistance has also been associated with exposure in pregnancy to raised concentrations of maternal glucocorticoids and permanent alteration in the offspring HPA axis is a likely mechanism underlying developmental programming in at least some of the animal models. The supposition that several of the models share characteristics of human metabolic syndrome is not entirely justifiable from the available data, as few laboratories study all of the constellation of disorders that contribute to this syndrome (insulin resistance, dyslipidaemia, hypertension, obesity). Amongst the nutritional models the development of hypertension is variable and dyslipidaemia is infrequently reported. It must also be considered that there are important difference in lipid metabolism between rodents and man. The recent observation that programmed disturbances of offspring’s stress responses are associated with hypomethylation status of the glucocorticoid receptor gene has fuelled speculation that altered methylation status may contribute to permanent programming of offspring gene expression and thence to phenotype. In addition, the transmission of certain phenotypic characteristics through the maternal line support a proposed role for permanent alteration in the mitochondrial genome. Imbalance of maternal nutrition may produce limits of tolerance in the offspring to nutritional challenge in later life (predictive adaptive responses). This intriguing hypothesis is one which can be put to the test in the different animal models.