The association between obesity and cardiovascular disease has been long established. More recently, the importance of the perivascular adipose tissue has been identified as a key mediator of vascular dysfunction (Van de Voorde et al., 2014). In addition to postnatal obesity, maternal obesity has also be shown to lead to long term changes in vascular function (Torrens et al. 2012; Stead et al. 2016) but whether maternal obesity alters the perivascular adipose remains unknown. The aim of this study was to investigate the effects of maternal and post-natal high fat diets on gene expression in perivascular adipose tissue. Female C57/BL6J mice 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=4-5 males). At 15 weeks of age, offspring were killed by cervical dislocation and perivascular fat from around the mesenteric arteries was dissected and snap frozen. Expression of genes involved in inflammation (IL6, CCL2, ChemR23) and adipokine signalling (adiponectin, cystathionine γ-lyase) were measured by qPCR. Data was analysed by 2-way-ANOVA for associations between prenatal and postnatal diet; significance was accepted at p<0.05. Post-natal high fat diet (CHF, HFHF) was associated with an increased expression of IL-6 (p<0.0005), CCL2 (p<0.05) and cystathionine γ-lyase (p<0.005) in perivascular adipose tissue relative to prenatal diets (CC, HFC). Expression of both the adipokine, adiponectin and the chemerin receptor (ChemR23) were similar across the four dietary groups (p>0.05). These data suggest that while a current obesogenic diet can impact upon expression in the perivascular adipose tissue, maternal obesity does not appear to be to lead to any long-term changes. Furthermore, the upregulation of IL-6 and CCL2 in the post-natal high fat groups fit with the previous findings that obesity leads to a pro-inflammatory phenotype.