Introduction: Obese pregnancies are not only associated with adverse consequences for the mother but also the long-term health of her child. Recent evidence from human studies has shown that individuals born to obese mothers are at increased risk of premature death from cardiovascular disease (CVD) in adulthood. Whilst important, such epidemiological studies fail to directly address causality. Our study aimed to address causality using a mouse model of maternal diet-induced obesity.Methods: Obesity was induced in female C57BL/6 mice using a diet high in simple sugars and saturated fat for 6 weeks prior to mating, throughout pregnancy and lactation. Control females were fed a standard laboratory chow diet throughout life. Male offspring from both groups were weaned onto chow and ex vivo cardiac function was studied in one per litter at 12 weeks of age by isolated Langendorff heart perfusion. Baseline measurements included left ventricular developed pressure, left ventricular end diastolic pressure and the minimum and maximum velocity of contraction. Both chronotropic and inotropic effects to muscarinic agonist carbachol and beta-adrenergic agonist isoprenaline were also assessed. Results: Cardiac hypertrophy was observed in offspring of obese dams from 3 to 8 weeks of age and was accompanied by an increase in cardiomyocyte cell area and re-expression of pathological cardiac fetal genes. At any time, there was no difference in offspring body weight between groups. At 12 weeks of age, offspring from obese dams had impaired systolic and diastolic function (Figure 1A-D) and cardiac sympathetic dominance (p<0.001). Conclusion: Maternal diet-induced obesity programmes cardiac dysfunction in the absence of any change in body weight and despite the fact that the offspring themselves had been eating a healthy low fat diet. These findings help to provide a causal link to explain and further support recent human observations linking maternal obesity to premature death from CVD.