Obesity prevalence is increasing in both the developed and developing world. This includes women of childbearing age, with recent UK statistics demonstrating that over half of women are now either overweight or obese during pregnancy. This is thought to contribute to the rising prevalence of gestational diabetes, with one in seven pregnancies globally estimated to be affected by this pregnancy condition. This is of concern as growing evidence suggests that, in addition to immediate detrimental consequences, developing in utero in an obesogenic/diabetic environment has a long-term impact on metabolic and cardiovascular health. This has been termed the Developmental Origins of Health and Disease and has been supported by studies in humans and in animal models. The strongest evidence from humans to suggest that development in utero in an obesogenic environment “programmes” increased risk of obesity and cardio-metabolic disease has come from the study of siblings born before and after maternal bariatric surgery [1]. These studies revealed that the sibling born after weight-loss surgery, when the mother was leaner, had reduced adiposity, lower blood pressure and increased insulin sensitivity compared to their sibling born prior to maternal weight-reducing surgery. We have used a mouse model of maternal diet-induced obesity to show that this relationship is causal and utilised it as a tool to define the mechanisms by which obesity during pregnancy impacts on the long-term cardio-metabolic health of the offspring [2]. In this model the obese dams have approximately double the adiposity of lean dams, are insulin resistant and develop impaired glucose in late gestation. Our studies have demonstrated that the offspring of obese dams develop insulin resistance, increased adiposity, cardiac dysfunction, hypertension and fatty liver when weaned onto a healthy low-fat diet. They are also more susceptible to diet-induced obesity. Characterisation of maternal physiology in the model identifies maternal hyperinsulinaemia as a key programming factor that could mediate the detrimental effects of maternal obesity on long-term health of the offspring [3]. Our findings therefore suggest that maternal insulin resistance may represent an important target of interventions to prevent the inter-generational transmission of poor cardio-metabolic health from mother to child. On-going studies are therefore exploring the effectiveness of maternal interventions known to improve maternal insulin sensitivity, such as increasing physical activity, as suitable approaches to improve both maternal and offspring health.