Abstract
Simple SummarySubclinical hypocalcemia severely affects the lactation and health of dairy cows. Subclinical hypocalcemia is still a concern with cows after postpartum oral Ca; thus, the single treatment approach gradually has shifted to a multitreatment approach in terms of subclinical hypocalcemia. Supplementing 25-hydroxyvitamin D3 could solve the problem of insufficient vitamin D3 synthesis and blocked conversion in transition cows. The present study showed that feeding 25-hydroxyvitamin D3 combined with oral calcium not only improved serum 25-hydroxyvitamin D3 status and calcium homeostasis, but also had potential benefits on lactation performance and the health status during the transition period.Little information is available regarding the effect of supplementing 25-hydroxyvitamin D3 during the transition period combined with a postpartum oral calcium bolus on Ca homeostasis. The objectives of the current study were to evaluate the effects of 25-hydroxyvitamin D3 combined with postpartum oral calcium bolus on lactation performance, serum minerals and vitamin D3 metabolites, blood biochemistry, and antioxidant and immune function in multiparous dairy cows. To evaluate the effects of 25-hydroxyvitamin D3 combined with oral calcium, 48 multiparous Holstein cows were randomly assigned to one of four treatments: (1) supplementing 240 mg/day vitamin D3 without a postpartum oral Ca bolus (control), (2) supplementing 240 mg/day vitamin D3 with an oral Ca bolus containing 90 g of Ca immediately post-calving (Ca + VitD), (3) supplementing 6 g/day 25-hydroxyvitamin D3 without an oral Ca bolus (25D), and (4) supplementing 6 g/day 25-hydroxyvitamin D3 with an oral Ca bolus containing 90 g of Ca immediately post-calving (Ca + 25D). Lactation performance during the first 21 days was measured. Blood was collected at the initiation of calving and then 1, 2, 7, 14, and 21 days relative to the calving date. The yield of milk (0.05 < p < 0.10), energy-corrected milk (p < 0.05), 3.5% fat-corrected milk (p < 0.05), and milk protein (p < 0.05) were significantly higher in 25-hydroxyvitamin D3-treated groups within 3 weeks of lactation than in vitamin D3-treated cows. The iCa (p < 0.05) and tCa (p < 0.05) were higher in both Ca and 25D + Ca cows than in the control and 25D groups within 48 h. The concentrations of serum tCa (p < 0.05), tP (p < 0.05), and 25-hydroxyvitamin D3 (p < 0.05) in 25D and 25D + Ca cows were higher than those in control and Ca cows within 21 days postpartum. Feeding 25-hydroxyvitamin D3 also showed a lower concentration of malondialdehyde (p < 0.05), interleukin 6 (p < 0.05), and tumor necrosis factor-alpha (TNF-α) (p < 0.05), as well as a higher concentration of alkaline phosphatase (p < 0.05), total antioxidant capacity (p < 0.05), and immunoglobulin G (p < 0.05) than vitamin D3. Supplementing Ca bolus also showed lower concentrations of alanine transaminase (p < 0.05) and TNF-α (p < 0.05). In conclusion, supplementing 25-hydroxyvitamin D3 during the transition period combined with a postpartum oral calcium bolus improved lactation performance, Ca homeostasis, and antioxidant and immune function of medium-production dairy cows within 21 days postpartum.
Highlights
During the transition period, hypocalcemia severely affects the health, lactation performance, and reproductive performance of dairy cows [1]
Low Ca diets and postpartum oral bolus Ca supplements have decreased the incidences of clinical hypocalcemia to a large extent, subclinical hypocalcemia has remained a prevalent issue in the cattle industry [2]
Our results suggested that 25-hydroxyvitamin D3 can be used in conjunction with an oral Ca bolus to potentially improve total Ca (tCa) during the first 3 weeks postpartum compared with a Ca bolus alone
Summary
Hypocalcemia severely affects the health, lactation performance, and reproductive performance of dairy cows [1]. In addition to decreased peripartal dry matter intake (DMI), hypocalcemia directly leads to milk fever and triggers other health disorders in cows, such as retained placenta, ketosis, displaced abomasum, metritis, and mastitis. Hypocalcemia was caused mainly by an abruptly increased Ca demand of colostrogenesis and subsequent milk production and delayed or disordered Ca mobilization. Strategies that could improve calcium mobilization or increase the blood concentration of calcium should be able to prevent hypocalcemia. In recent years, increased attention has been directed toward postpartum oral Ca boluses for preventing the occurrence of hypocalcemia. This strategy of Ca delivery is feasible because Ca is absorbed by passive diffusion through the junctions connected with mucosal cells that depend on Ca concentrations in the lumen [2].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
