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It has been established that essential amino acids (EAA) regulate protein synthesis in mammary epithelial cells by rapidly altering the phosphorylation state of translation factors. However, the long-term transcriptional response to EAA supply has been investigated much less. Eight transcription factors were selected as candidate mediators of EAA effects on mammary cell function via the amino acid response (ATF4, ATF6), mitogen-activated protein kinase (JUN, FOS, EGR1), and mechanistic target of rapamycin complex 1 (MYC, HIF1A, SREBF1). The objective was to determine if and when expression of these candidate genes was affected in primary cultures of bovine mammary epithelial cells more than 24 h after imposing an EAA deficiency, and to evaluate effects of EAA deficiency on protein synthesis, endoplasmic reticulum size, cell proliferation, and lipogenesis. Differentiated cells were cultured in 1 of 3 treatment media representing normal physiological concentrations of all amino acids (CTL), low lysine (LK), or low methionine (LM) for 24, 40, 48, or 60 h. Both LK and LM suppressed protein synthesis and activated ATF4 expression, indicating the classic amino acid response pathway had been triggered. However, there was no effect of LK or LM on endoplasmic reticulum size, possibly related to elevated ATF6 expression on LM. Expression of early response genes JUN, FOS, EGR1 and MYC was not elevated by EAA deficiency but LM decreased EGR1 expression. LM also increased expression of HIF1A. The EGR1 and HIF1A expression results are consistent with the decrease in cell proliferation rate observed. Variable responses in SREBF1 expression to LK and LM at different timepoints may have contributed to a lack of effect on lipogenesis rates. These findings indicate that EAA deficiency may inhibit mammary protein synthesis and cell proliferation through transcription factors. [ABSTRACT FROM AUTHOR]

The ruminant is able to transform plant fibres and non‐protein nitrogen (NPN) into edible foods for human consumption. In an effort towards improving our understanding of this process, we sought to challenge convention and examine how the source, amount and site of NPN delivery in the gastrointestinal tract of the ruminant may affect fibre digestibility, rumen stability and N metabolism. In the first study presented here, we used four ruminally cannulated non‐lactating heifers in a Latin square design to infuse 59 g/days of N in the form of ammonia (A) or urea (U) into either the rumen (R) or the abomasum (A). We found that intake was higher (p =.03) for animals receiving supplementary NPN as urea compared with ammonia. In addition, abomasally infused urea (UA) improved fibre fermentation by 9.4% (p =.05) and decreased ruminal pH fluctuations (lower slope in the cumulative pH parameters, p =.04) when compared with the same amount of urea infused ruminally (UR). In a second study, using the same group of heifers, we infused 50 or 150 g/day of urea into the rumen (UR50 and UR150) or 150 g of urea in the abomasum (UA150) or 50 g in the rumen and 100 g in the abomasum (URA150). Fibre digestion was improved by 4% (p =.02) when the same dose of urea was infused into the abomasum compared with the rumen, while estimated microbial protein production and N efficiency were not different between a low rumen dose and high post‐ruminal dose of urea. Collectively, these studies provide insight into the viability of post‐ruminal NPN supplementation as a strategy to improve fibre digestion and NPN inclusion in the ruminant diet. [ABSTRACT FROM AUTHOR]

Gluconate salts have been reported to be metabolized by microbes in the gastrointestinal tract to yield butyrate and consequently enhance its functionality. The objective was to evaluate feed intake, growth, and carcass characteristics for heifers fed increasing doses of hydrogenated fat-embedded calcium gluconate (HFCG). Twenty-one 10-mo Simmental × Limousin beef heifers, blocked by initial BW (323 ± 35.3 kg), were individually fed for 206 d (8.72% barley silage, 87.44% dry-rolled barley grain, and 3.84% mineral and vitamin supplement) and used to evaluate three different levels of HFCG (0.0%, 0.09%, and 0.18%; on DM basis through substitution of barley grain). Dry matter intake was determined weekly, and BW was measured at the start and end of the study and every three weeks. Carcass weight was recorded and carcasses were refrigerated for 13 d. The left ribeye (10th to 13th rib) was excised and evaluated by a certified grader from the Canadian Beef Grading Agency. Inclusion of HFCG did not affect DMI (8.29 kg/d; P = 0.87), ADG (1.37 kg/d; P =0.55), or G:F (0.166 kg/kg; P = 0.32). Final live BW and carcass weight averaged 630.9 ± 34.99 and 374.1 ± 10.19 kg and were not affected by treatment (P = 0.73 and 0.65, respectively). Dose of HFCG did not affect carcass characteristics with average values of 7.0 mm for fat thickness (P = 0.46), 104 cm2 for rib-eye area (P = 0.92), 476 for marbling score (P = 0.94), and 50.3% for retail cut yield (P = 0.62). In addition, HFCG did not affect quality grade (P = 0.38) or yield grade (P = 0.86). The present data suggests that the use of HFCG did not affect performance of finishing heifers or carcass quality on beef heifers regardless of dose. [ABSTRACT FROM AUTHOR]