Circadian (24-h) and feeding-fasting rhythms are major regulators of liver physiology, but how these daily rhythms shape hepatic function, and how this regulation changes in metabolic disease, remains incompletely understood. We recently found that the timing of food intake strongly influences daily rhythms in the hepatic secretome in both humans and mice, suggesting that feeding rhythms are an important determinant of liver-derived systemic signals. To understand the underlying mechanism, we investigated daily regulation of the hepatic secretory machinery. Temporal proteomics revealed pronounced rhythmicity in pathways controlling protein folding and glycosylation within the ER and Golgi, which depended on an intact molecular circadian clock. We subsequently identified hepatic glycogen metabolism as a key link between feeding and protein secretion. Glycogen breakdown supplies metabolites required for protein glycosylation, while disruption of this process alters ER homeostasis and dampens rhythmic protein secretion. We further found that this regulatory pathway is impaired in ob/ob mice, linking disruption of daily hepatic secretory function to obesity-associated steatosis and metabolic dysfunction. Together, our findings reveal how circadian and feeding rhythms converge on glycogen metabolism to regulate hepatic protein secretion. Our ongoing work investigates how disruption of these mechanisms contributes to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD).