Obesity is a major global health concern and associated with a range of cardiometabolic disease. More recently, it has been linked to respiratory diseases such as asthma and COPD (Reilly et al., 2003). Beyond direct reproductive consequences, maternal obesity has proven associations with increased prevalence of respiratory disease in the offspring. Specially, children born to obese mothers are more likely to suffer respiratory infections and childhood wheeze (Haberg et al., 2009). The aim of this project was to investigate the impact of maternal obesity and early postnatal diet upon the expression of genes associated with lung: development, architecture and function, in the lungs of offspring. Female C57/BL6J mice (n=29) were fed either standard chow (C; 7% kcal fat, 18% kcal protein, 75% carbohydrates) or an obesogenic high-fat diet (HFD; 45% kcal fat, 17% kcal protein, 35% kcal carbohydrates) for 4-6 weeks prior mating and throughout gestation and lactation. At weaning, pups were transferred to either C or HFD to give four dietary phenotypes, CC, HFC, CHF & HFHF (n=4-6 males and females per group). Offspring were killed by cervical dislocation at 30 weeks of age and the lungs were snap frozen. Expression of genes involved in inflammation (IL6, IL33 & TNFa), remodelling (TGF-b2 & ADAM33) and obesity (FTO) were measured by quantitative real-time RT-PCR. Data was analysed by 2-way-ANOVA for associations between prenatal and postnatal diet; significance was accepted at p<0.05. Increased ADAM33 expression was seen in lungs of male mice born to obese dams (prenatal HFD mice) compared with prenatal C mice (p<0.012, F=2.299). Increased FTO expression was seen in lungs of male postnatal HFD mice compared with postnatal C mice (p<0.013, F=0.544). Decreased expression of IL6 was seen in the lungs of male postnatal HFD mice compared with postnatal C mice (p<0.023, F= 0.824). No changes were seen in levels of TNF-a, TGF-b2 and IL-33. These data suggest that both maternal and postnatal obesity differentially alter gene expression in the offspring lung. That similar changes in these genes have previously been associated with impaired lung function suggests that maternal obesity alone can lead to long term respiratory changes.