The on-going obesity epidemic has seen an increase in the prevalence of non alcoholic fatty liver disease (NAFLD). We have previously shown that maternal high fat diets (mHFD) can increase the susceptibility of developing a severe form of NAFLD (non-alcoholic steatohepatitis or NASH) in adulthood, through increased lipogenesis gene expression and mitochondrial dysfunction. Components of the endogenous molecular “clock” network transcriptionally regulate genes involved in mitochondrial and fatty acid metabolism through time-of-day dependant negative feedback loops. Therefore we investigated whether early HF exposure in rodents could disrupt the expression of hepatic clock genes (Cry1, Cry2) and genes important for mitochondrial fatty acid metabolism (Sirt3), to cause metabolic changes that promote NASH development in adulthood. Rodent dams were fed a control (C) or HF diet before and during gestation and lactation. Offspring were fed either the C or HF diet after weaning to generate 4 offspring groups: HF/HF, HF/C, C/HF and C/C. Livers of 15 week old male offspring were obtained during the day (ZT8 = 3 pm) and night (ZT20 = 3 am). Expression of the genes: Cry1, Cry2 and Sirt3 were measured by quantitative PCR. We observed a significant reduction (3.3-fold decrease) in night-time Cry1 expression in the HF/C offspring (p<0.05). In addition, mHFD exposure (HF/C offspring) appeared to reverse the canonical day-night gene expression pattern in these offspring, and a there was a trend towards elevated night-time Cry2 expression (p=0.1). Moreover, there was a significant reduction (12.5-fold decrease) of night-time Sirt3 gene expression in the HF/HF offspring (p<0.05). In summary, these results illustrate that exposure to a mHFD induces day-night changes in hepatic core clock gene expression. We suggest that lower expression of Cry2 during the day in offspring exposed to a mHFD may result in altered transcriptional regulation of other clock components resulting in downstream perturbations in hepatic metabolism. In addition, mHFD exposure coupled with HF exposure in later life decreased Sirt3 expression. This may provide a potential mechanism underlying the developmental priming of mitochondrial impairment leading to NASH onset.