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Circadian disruption increased insulin resistance and decreased mammary development in late gestation, nonlactating (dry) cows. The objective was to measure the effect of circadian disruption on transcriptomes of the liver and mammary gland. At 35 days before expected calving (BEC), multiparous dry cows were assigned to either control (CON) or phase-shifted treatments (PS). CON was exposed to 16-h light and 8-h dark. PS was exposed to 16-h light to 8-h dark, but phase of the light-dark cycle was shifted 6 h every 3 days. On day 21 BEC, liver and mammary were biopsied. RNA was isolated ( n = 6 CON, n = 6 PS per tissue), and libraries were prepared and sequenced using paired-end reads. Reads mapping to bovine genome averaged 27 ± 2 million and aligned to 14,222 protein-coding genes in liver and 15,480 in mammary analysis. In the liver, 834 genes, and in the mammary gland, 862 genes were different (nominal P < 0.05) between PS and CON. In the liver, genes upregulated in PS functioned in cholesterol biosynthesis, endoplasmic reticulum stress, wound healing, and inflammation. Genes downregulated in liver function in cholesterol efflux. In the mammary gland, genes upregulated functioned in mRNA processing and transcription and downregulated genes encoded extracellular matrix proteins and proteases, cathepsins and lysosomal proteases, lipid transporters, and regulated oxidative phosphorylation. Increased cholesterol synthesis and decreased efflux suggest that circadian disruption potentially increases the risk of fatty liver in cows. Decreased remodeling and lipid transport in mammary may decrease milk production capacity during lactation.

Metabolizable protein supply is a limiting factor for milk production in dairy cows, and the availability of AA is a function of the quantity of the metabolizable protein available and of hepatic AA catabolism. This study aimed to evaluate the effect of postruminal protein infusion on key genes for ureagenesis and AA catabolism. Six multiparous Holstein cows in early lactation were used in a replicated crossover design. Cows were fed a TMR and infused postruminally with either 0 or 600 g/d of milk protein isolate. Periods were 21 d long, consisting of 14 d of adjustment to surroundings, followed by 7 d of protein infusion. On the last day of each infusion, liver samples were collected for mRNA analysis and explant culture, milk samples were collected for mRNA analysis, and blood samples were collected for plasma metabolite analysis. Postruminal infusion of protein increased milk yield by 10.5%, milk fat yield by 12.5%, milk protein yield by 20%, milk lactose yield by 11%, and total solids yield by 15.5%. Postruminal infusion of protein increased milk urea N by 23.5%, blood urea N by 18.6%, and the abundance of hepatic ornithine transcarbamoylase mRNA by 52.8%. Postruminal infusion of protein did not alter the mRNA abundance of hepatic argininosuccinate synthase, α-aminoadipate semialdehyde synthase, cysteine sulfinic acid decarboxylase, or cystathionase. The abundance of RNA for milk proteins was unchanged with postruminal protein infusion. Metabolism of l -[U 14C] Lys to CO2 was increased by 127% (0.143 vs. 0.063 ± 0.04 nmol product·mg tissue−1·h−1), and the metabolism of l -[U 14C] Ala to CO2 increased by 40.5% (0.52 vs. 0.37 ± 0.06 nmol product·mg tissue−1·h−1) with postruminal protein infusion. The rate of l -[1-14C] Met oxidation did not differ. These data indicate increased ureagenesis matched by upregulation of nonessential AA catabolism and a disproportional increase in Lys oxidation in response to increased postruminal protein infusion.