Excess prenatal glucocorticoid exposure predisposes offspring to an adverse metabolic phenotype, including altered adipose tissue gene expression and can lead to obesity and type 2 diabetes. Clock genes are now recognized as key regulators of metabolic function in a range of tissues, but the impact of programming insults on their expression is unknown. The aim of this study was to determine if circadian variation in adipose and liver tissue expression of clock genes is programmed by prenatal glucocorticoids. Furthermore, we investigated whether postnatal high-fat (HF) diet (± omega-3 (n-3) fatty acid supplementation) further modifies programmed outcomes. Rats were either untreated (Con; n=24) or dexamethasone treated (0.5 μg/ml in drinking water; Dex, n=24) from pregnancy day 13 to term (day 23). Offspring were cross-fostered to untreated mothers and males were weaned onto either a standard (Std), a HF or HF, high n-3 (HFHn3) diet. After 6 months, tissues were collected at four Zeitgeber times (ZT1=8am, ZT7=2pm, ZT13=8pm and ZT19=2am; each n=8). Plasma insulin and glucose, and circadian expression of hepatic and retroperitoneal fat clock genes and PPAR genes were measured. Prenatal Dex elevated offspring glucose (p<0.05), tended to increase insulin levels (p=0.061) and suppressed adipose tissue expression and rhythmicity of Clock, Bmal1, Per1 and Per3 (p<0.01). HF consumption suppressed expression of Per1, Per2 and Cry1 (p<0.01) in adipose tissue. Supplementation with n-3 partially corrected HF-induced changes in adipose tissue clock genes (Per1, Per2, and Cry1; p<0.05). In conclusion, prenatal Dex treatment programmed perturbations in plasma glucose and insulin profiles and adipose tissue clock gene expression. While a postnatal HF diet amplified this phenotype, supplementation with n-3 reduced the impact of both programming and the HF diet. We conclude that changes in clock gene rhythmicity and glucose sensitivity may underlie glucocorticoid programming of adipose tissue metabolism.