It is well established that events in fetal and neonatal life can influence an individual’s risk of developing metabolic conditions such as type 2 diabetes, insulin resistance and cardiovascular disease in later life. Much of the early focus of such “programmed” events was directed towards the effects of maternal under-nutrition and low birth weight on the long-term health of an individual. However in light of the growing epidemic of obesity, including in women of child-bearing age, attention has now been directed towards understanding the effects of maternal over-nutrition during pregnancy and lactation on the long-term health of the offspring1. To address this we, and others, have used a mouse model of maternal diet-induced obesity where pregnant and lactating mice are fed a diet rich in saturated fats and simple sugars (reflective of a human westernized diet) to induce obesity prior to pregnancy. This maternal dietary manipulation leads to cardiovascular dysfunction2 and insulin resistance in the offspring that is associated with post-transcriptional programming of insulin signaling protein expression3. The offspring of obese dams are also more susceptible to diet induced obesity. As well as utilizing the mouse model as a tool to identify mechanisms through which programmed changes in the offspring arise, we have also utilized it to identify factors in the obese mother that mediate the detrimental effects in the offspring. Maternal hyperinsulinaemia, which is amenable to lifestyle interventions such as increased physical activity, has emerged as one important parameter. These findings in an animal model therefore provide important insight into rational intervention strategies that have the potential to prevent transmission of metabolic dysfunction between generations.