The liver is an essential organ regulating metabolic homeostasis in response to fluctuations of metabolites induced by daily rhythms of food intake. Homeostasis is maintained by precise dynamic regulation of signaling pathways controlling a wealth of enzymatic reactions regulating lipid, bile acid, xenobiotic, amino acid and glucose metabolism in hepatocytes. Here, precise temporal expression of hepatic enzymes is crucial, where a major part of circadian hepatic protein expression is regulated by precisely timed gene transcription (1). This is controlled by complex interactions between rhythmic endocrine signaling, oscillating metabolites and intrinsic circadian networks (2). Genetic disruption of the intrinsic circadian clock has profound impact on circadian gene transcription in liver, yet rhythmic gene transcription can be restored by controlled feeding regimens (3-5), likely regulated by putative food-entrainable oscillators (6). We aim to understand mechanisms controlling circadian hepatic gene expression with a specific focus on molecular cues coming from daily feeding cycles. The experimental approaches are centered on functional genomics technologies seeking to characterize differential transcriptomic and cistromic regulation in response to food intake. We use a mouse model, where C57BL/6 mice are trained to night restricted feeding in a 12-hour day/night cycle (food available from ZT12 to ZT24). At the day of the experiment we collect livers from various pre- and post-prandial timepoints. To measure the effect of feeding we keep a cohort of mice unfed from ZT12-ZT24. Using integrated RNA-seq, DNase-seq and H3K27Ac ChIP-seq analysis we can identify hundreds of circadian regulated genes and enhancers controlled by feeding. Bioinformatic analysis of the putative feeding regulated enhancers suggests a functional role of transcription factors such as GR, FOXO1, CREB and HNF4. Focusing on feeding repressed gene expression shows that post-prandial suppression of enhancer activity is associated with reduced genome-wide GR and FOXO1 occupancy of chromatin correlating with reduced serum corticosterone levels and increased serum insulin levels. Despite substantial pre-prandial co-occupancy of feeding regulated enhancers by GR and FOXO1, selective genetic or pharmacological disruption of post-prandial corticosteroid or insulin signaling demonstrates that these signaling pathways selectively operate specific feeding regulated gene programs. Importantly, combined regulation of these signaling pathways showed to be a major determinant of repressed gene expression in response to feeding (7). Interestingly, genetic disruption of the glucocorticoid receptor in liver also perturbed a subset of genes induced by feeding, including Gck important for glucose uptake by the liver. Using primary hepatocytes, we find that glucocorticoid pre-treatment is necessary for subsequent insulin induced Gck expression and ChIP shows GR occupancy of two enhancers near the Gck gene in liver and primary hepatocytes. This suggest that Gck is directly regulated by GR and indicate that glucocorticoids and insulin cooperate to repress and induce post-prandial gene expression in the liver.