Twelve lactating Holstein cows (132 ± 21 days in milk) were enrolled in a Latin square experiment to explore the extent to which source and amount of supplemental dietary Zn can impact barrier function of mammary epithelial tissue. Cows received either 970 mg supplemental Zn/day as ZnSO 4 (LS), 1,640 mg supplemental Zn/day as ZnSO 4 (HS), or 1,680 mg supplemental Zn/day as a mixture of ZnSO 4 and Zn methionine complex (HC). Treatments lasted for 17 days followed by 4 days of sample collection. Blood and milk were collected and analyzed for markers of blood-milk leak including plasma lactose and αlactalbumin and milk electrolytes. Total RNA was also isolated from milk cells and abundance of Zn transporter 2 (ZnT2) and clusterin, genes with potential impact on Zn-dependent apoptosis and cell survival, were measured. Finally, dairy food properties of milk (heat coagulation time, nonprotein nitrogen, and noncasein nitrogen) were also analyzed. Cows on the HS treatment tended to have higher feed intake than LS (P = 0.06), and milk fat percentage tended to increase for HC compared to LS (P = 0.08). No other effects on milk composition, yield, or production efficiency were observed. No effects were observed on markers of blood-milk leak, mRNA abundance of ZnT2 or clusterin, or dairy food chemistry properties. Concentration and source of dietary Zn did not impact mammary epithelial integrity in lactating cows during late lactation. SummaryTwelve lactating Holstein cows (132 ± 21 days in milk) were enrolled in a Latin square experiment to explore the extent to which source and amount of supplemental dietary Zn can impact barrier function of mammary epithelial tissue. Cows received either 970 mg supplemental Zn/day as ZnSO 4 (LS), 1,640 mg supplemental Zn/day as ZnSO 4 (HS), or 1,680 mg supplemental Zn/day as a mixture of ZnSO 4 and Zn methionine complex (HC). Treatments lasted for 17 days followed by 4 days of sample collection. Blood and milk were collected and analyzed for markers of blood-milk leak including plasma lactose and α-lactalbumin and milk electrolytes. Total RNA was also isolated from milk cells and abundance of Zn transporter 2 (ZnT2) and clusterin, genes with potential impact on Zn-dependent apoptosis and cell survival, were measured. Finally, dairy food properties of milk (heat coagulation time, nonprotein nitrogen, and noncasein nitrogen) were also analyzed. Cows on the HS treatment tended to have higher feed intake than LS (P = 0.06), and milk fat percentage tended to increase for HC compared to LS (P = 0.08). No other effects on milk composition, yield, or production efficiency were observed. No effects were observed on markers of blood-milk leak, mRNA abundance of ZnT2 or clusterin, or dairy food chemistry properties. Concentration and source of dietary Zn did not impact mammary epithelial integrity in lactating cows during late lactation.
Two studies were designed to evaluate the relative bioavailability of l-carnitine delivered by different methods in dairy cattle. In experiment 1, 4 Holstein heifers were used in a split-plot design to compare ruminally or abomasally infused l-carnitine. The study included 2 main-plot periods, with infusion routes allocated in a crossover design. Within main-plot periods, each of 3 subplot periods consisted of 4-d infusions separated with 4-d rest periods. Subplot treatments were infusion of 1, 3, and 6 g of l-carnitine/d in conjunction with 6 g/d of arabinogalactan given in consideration of eventual product manufacturing. Doses increased within a period to minimize carryover risk. Treatments were solubilized in 4 L of water and delivered in two 10-h infusions daily. Blood was collected before the start of infusion period and on d 4 of each infusion period to obtain baseline and treatment l-carnitine concentrations. There was a dose × route interaction and route effect for increases in plasma carnitine above baseline, with increases above baseline being greater across all dose levels when infused abomasally compared with ruminally. Results demonstrated superior relative bioavailability of l-carnitine when ruminal exposure was physically bypassed. In experiment 2, 56 lactating Holstein cows (143 ± 72 d in milk) were used in 2 cohorts in randomized complete block designs (blocked by parity and milk production) to evaluate 2 rumen-protected products compared with crystalline l-carnitine. Treatments were (1) control, (2) 3 g/d of crystalline l-carnitine (crystalline), (3) 6 g/d of crystalline, (4) 5 g/d of 40COAT (40% coating, 60% l-carnitine), (5) 10 g/d of 40COAT, (6) 7.5 g/d of 60COAT (60% coating, 40% l-carnitine), and (7) 15 g/d of 60COAT. Treatments were top-dressed to diets twice daily. Each cohort used 14-d and included a 6-d baseline measurement period with the final 2 d used for data and sample collection, and an 8-d treatment period with the final 2 d used for data and sample collection. Plasma, urine, and milk samples were analyzed for l-carnitine. Crystalline and 40COAT linearly increased plasma l-carnitine, and 60COAT tended to linearly increase plasma l-carnitine. Total excretion (milk + urine) of l-carnitine averaged 1.52 ± 0.04 g/d in controls, increased linearly with crystalline and 40COAT, and increased quadratically with 60COAT. Crystalline increased plasma l-carnitine and l-carnitine excretion more than 40COAT and 60COAT. In conclusion, preventing ruminal degradation of l-carnitine increased delivery of bioavailable carnitine to cattle, but effective ruminal protection and postruminal bioavailability is challenging.
Dairy cattle are subjected to oxidative stress, inflammation, and altered immune function during the transition to lactation. The objective of this study was to evaluate the effects of a dietary Saccharomyces cerevisiae fermentation product (SCFP; NutriTek, Diamond V) on oxidative status, inflammation, and innate and adaptive immune responses during the transition period. Holstein cows were blocked by parity, expected calving date, and previous milk yield and then randomly assigned to treatment within block. Treatment was a control total mixed ration (n = 30) or SCFP total mixed ration (n = 34) fed from −29 ± 5 to 42 d relative to calving (RTC). Blood was sampled during wk −4, −2, 1, 2, and 5 and liver tissue at wk −3 and 2 RTC. Oxidative status was evaluated in plasma by retinol, α-tocopherol, and malondialdehyde concentrations, glutathione peroxidase activity, and Trolox equivalent antioxidant capacity, and in liver by mRNA abundance of nuclear factor E2-related factor 2 (NFE2L2), metallothionein 1E (MT1E), and glutathione peroxidase 3 (GPX3). Inflammation was evaluated in plasma by haptoglobin (HP) and serum amyloid A (SAA) concentrations and in liver by mRNA abundance of HP, serum amyloid A3 (SAA3), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB1). Innate immune response was measured by stimulated oxidative burst of polymorphonuclear cells (neutrophils) isolated from blood. Ovalbumin (OVA) was administered with adjuvant on d 7 and 21 RTC, and adaptive immune response was evaluated by serum anti-OVA IgG content on d 28 and 35. Mixed models were used to assess effects of treatment, time, parity, and all interactions. We previously reported that SCFP had limited effects on productivity in this cohort, although milk fat yield was transiently increased and subclinical ketosis incidence was increased. Supplementation with SCFP did not affect overall oxidative, inflammatory, or immune parameters. The only treatment × week interaction detected was for plasma α-tocopherol concentration, which tended to be greater in control cows during wk 2 RTC. A tendency for a treatment × parity interaction was detected for serum anti-OVA IgG titer, which tended to be greater for SCFP than for controls among primiparous cows. Plasma inflammatory biomarkers were not affected by SCFP but, unexpectedly, plasma HP was elevated at both prepartum time points and plasma SAA was elevated during wk −2 RTC compared with the expected increases in both biomarkers postpartum. In this cohort of transition cows with low disease incidence, SCFP generally did not affect oxidative, inflammatory, or immune parameters.
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