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.

ABSTRACTTwo 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.

Objectives of this study were to determine effects of supplemental zinc level and source on mammary epithelial barrier integrity and milk chemistry in dairy cattle. In a mouse model, moderate zinc deficiency was shown to dramatically impact milk secretion and mammary gland involution. In addition, through multiple pathways, zinc is known to impact apoptosis in mammary and other epithelial tissues. To test for similar effects in cattle, 12 multiparous Holstein cows in mid to late lactation (132 ± 21 DIM) were blocked by milk production and randomly assigned to treatment sequence in a replicated 3 × 3 Latin square experiment. Each treatment period lasted 21 d (17 d of acclimation and 4 d of sampling). Treatments consisted of 1) 0.97 g zinc/d provided as ZnSO4 (approximately 30 mg zinc/kg diet DM; 30-ZS), 2) 1.64 g zinc/d as ZnSO4 (60-ZS), and 3) 0.55 g zinc/d provided as ZnSO4 plus 1.13 g zinc/d provided as a zinc methionine complex (60-ZM; Zinpro Corp., Eden Prairie, MN). Treatments were also balanced for metabolizable methionine using Smartamine M (Adisseo Inc., France). Cows were housed in individual tie stalls, given ad libitum access to water, and fed a balanced basal ration twice daily. Treatments were provided daily in an oral bolus and contained all supplemental trace minerals except for selenium, which was included in the grain mix. Measurements were analyzed with a mixed model using fixed effects of treatment, period, and their interaction and the random effect of cow. Significance was declared at P < 0.05 and tendencies at P < 0.10. Feed intake tended to increase for 60-ZS cows (P = 0.06) and 60-ZM cows tended to have increased milk fat percentage (P = 0.08) compared with 30-ZS cows. No other effects on milk composition, yield, or production efficiency were observed. No effects of treatments were observed on heat coagulation time or the percent of NPN in the milk. Plasma electrolyte, lactose, and α-lactalbumin levels as well as transcript abundance of genes implicated in zinc transport (ZnT2), tight junction formation (occludin), and apoptosis (clusterin) were also unaffected by treatment. In conclusion, zinc supplementation of dairy rations at 60 ppm as opposed to 30 ppm did not appear to impact the integrity of the blood milk barrier or dairy food properties of milk.