Perturbations in circadian rhythms are associated with a range of metabolic disorders including obesity, type 2 diabetes and fatty liver disease. We have previously shown that high fat (HF) exposure during early life primes adult onset of severe fatty liver in the offspring. Recent findings show that hepatic lipid homeostasis is maintained by a cell autonomous transcriptional feedback loop composed of the transcription factors CLOCK and BMAL1 and their target genes many of which are transcription factors with roles in lipogenesis (e.g REVERB, SREBP1c). Therefore, the precise timing of clock gene expression is critical for optimal hepatic metabolism. The “clock” proteins are regulated by the NAD+ dependent deacetylase SIRT1, and thus are themselves influenced by nutrition and cellular metabolism. To date, the effect of HF exposure during early life on the circadian clock network and hepatic metabolism in the offspring in later life is unknown. We used our mouse model of developmentally primed fatty liver disease to demonstrate that offspring exposed to HF diets during development and adulthood exhibit the most severe fatty liver phenotype in later life. These offspring also show a reduction in cellular NAD+ and SIRT1 expression. We show that the circadian pattern of core clock genes, and protein expression, is disrupted in response to a HF diet a perturbation that is exacerbated in offspring exposed to a maternal HF diet during development. Moreover, expression of clock target genes involved in lipogenesis (REVERB, SREBP1c) is up-regulated in offspring from HF fed mothers, which may further contribute to fat accumulation in the liver. Our results suggest that early HF exposure causes persistent changes in cellular redox status, SIRT1 reduction, clock gene imbalance, and up-regulated lipogenic transcription factors, developmentally priming the onset of fatty liver in later life.