Introduction: Obesity now affects nearly 1 in 3 adults in the UK. It is estimated that 20% of pregnant women are obese. Increasing evidence associate obesity in pregnancy with susceptibility to obesity and metabolic syndrome in the child. Here we employ an established mouse model of maternal obesity [1] to investigate energy balance and glucose metabolism in the offspring. Polydextrose (PDX) has been shown to improve glucose metabolism [2] and, therefore may be beneficial in obese pregnancy.Hypothesis: We hypothesised that (a) maternal obesity has adverse effects on offspring energy balance and glucose metabolism and that (b) these adverse effects will be prevented by supplementation of the maternal diet with PDX. Moreover, we investigated whether PDX supplementation in obese pregnancy is protective against the adverse influences of an obesogenic dietary exposure in adulthood.Methods: Female mice were fed a control or an obesogenic diet [1], 6-weeks before mating and throughout pregnancy and lactation. A cohort of the obese dams was assigned to supplementation with 5% PDX in pregnancy and lactation. Offspring were weaned onto control diet. At 3 and 6 months of age energy intake (EI), energy expenditure (EE) and Respiratory Exchange Ratio (RER) were measured by indirect calorimetry, (Labmaster, TSE) and glucose-tolerance-tests were performed. At 3 months some of the animals were challenged for 3-weeks with an obesogenic diet before re-estimation of EI, EE, and RER. Results: At 3 months of age, offspring of obese dams (OffOb) metabolic parameters did not differ from offspring of control dams (OffCon). At 6 months OffOb were heavier (P<0.01), had lower RER (P<0.05) and lower EE (P<0.001) compared to OffCon. OffOb had impaired glucose metabolism compared to OffCon (P<0.05). Maternal supplementation with PDX prevented these defects. Following 3 weeks obesogenic dietary challenge OffObs demonstrated hyperphagia and greater increase in bodyweight than controls (P<0.05),which was prevented by maternal PDX supplementation. PDX also normalized the reduction in EE observed in OffOb after the obesogenic dietary challenge (P< 0.05). Conclusions: Maternal obesity was associated with increased bodyweight in offspring at 6 months of age, which we attribute to decreased EE. Maternal administration of PDX prevented the effects of maternal obesity on offspring energy balance and glucose metabolism. Maternal supplementation with PDX protected OffObs from developing hyperphagia and decreased EE, which lead to increased weight gain following exposure to obesogenic diet in adulthood. Maternal obesity adversely influences offspring energy balance, which is prevented by maternal intervention with PDX. PDX may, therefore, provide a potential therapeutic intervention in preventing the transgenerational acceleration of obesity.