Around parturition, many dairy cows experience varying degrees of hypocalcemia, which increases the incidence of several diseases in early lactation. In the current study, an established concept of feeding a diet negative in cation-anion difference (DCAD) was combined with oral supplementation of 25-hydroxyvitamin D(3) (25-OHD(3)) from d 270 of gestation until parturition. Fifty-six dairy cows were divided into 2 feeding groups (low DCAD and control). Fourteen animals of each group received a daily dosage of 3mg of 25-OHD(3). From the beginning of the treatment to d 10 after parturition, plasma samples for analysis of 25-OHD(3), 1,25-dihydroxyvitamin D(3), parathyroid hormone (PTH), Ca(2+), phosphate, the bone resorption marker CrossLaps, and osteocalcin were collected every other day, at calving, and at 6, 12, and 24h after calving. Urine samples for determination of macrominerals and measures of acid-base status were collected on d 6 of treatment and on d 6 after calving. The induction of a compensated metabolic acidosis by the animals on the DCAD diet could be demonstrated by decreased urinary pH. A linear correlation between treatment duration and the plasma concentration of 25-OHD(3) indicated effective absorption of 25-OHD(3) in supplemented animals. The mean plasma concentrations of Ca(2+) from d -4 prepartum to d 4 postpartum were significantly higher in animals treated with the combination of the low DCAD diet and 25-OHD(3) supplementation (1.24±0.02 mmol/mL) compared with the 3 other groups (low DCAD: 1.17±0.02 mmol/mL; control diet plus 25-OHD(3): 1.16±0.02 mmol/mL; control diet: 1.18±0.02 mmol/mL). We postulate that the increased tissue responsiveness to parathyroid hormone induced by the low DCAD is crucial for the observed positive effects of the 25-OHD(3) treatment.
Holstein cows (>1 gestation) were fed 1 of 3 diets during the last 13 d of gestation (ranged from 22 to 7 d). The control diet (16 cows) was formulated to provide 18,000 IU/d of vitamin D3 and had a dietary cation-anion difference (DCAD) of 165mEq/kg (DCAD=Na + K - Cl - S). The second diet (DCAD + D) provided the same amount of vitamin D3 but had a DCAD of -139mEq/kg (17 cows). The third diet (DCAD + 25D) had no supplemental vitamin D3 but provided 6mg/d of 25-(OH) vitamin D3 [25-(OH)D3] with a DCAD of -138mEq/kg (20 cows). Diets were fed until parturition and then all cows were fed a common lactation diet that contained vitamin D3. Negative DCAD diets reduced urine pH, with the greatest decrease occurring with the DCAD + D treatment. Urinary Ca excretion was greatest for cows fed DCAD + 25D followed by cows fed DCAD + D. Urinary pH was negatively correlated with urinary excretion of Ca for cows fed DCAD + D. No such correlation was observed with the DCAD + 25D treatment because substantial excretion of urinary Ca occurred at moderate urinary pH values for that treatment. Cows fed DCAD + 25D had greater serum concentrations of 25-(OH)D3 than other treatments from 5 d after supplementation started through 7 d in milk. Concentrations of 1,25-(OH)2D3 in serum were greatest in DCAD + 25D cows starting at 2 d before calving and continued through 7 d in milk. Serum Ca concentrations 5 d before calving were greatest for cows fed DCAD + 25D, but at other time points before and after parturition treatment did not affect serum Ca. Incidence of clinical hypocalcemia was not statistically different between treatments, but cows fed DCAD + 25 had the highest incidence rate (12.5, 0, and 20% for control, DCAD + D, and DCAD + 25D). Calves born from cows fed DCAD + 25D had greater concentrations of 25-(OH)D3 in serum at birth than calves from other treatments (before colostrum consumption), but concentrations were similar by 3 d of age. Concentrations of 25-(OH)D3 in colostrum and transition milk were increased by feeding DCAD + 25D, but by 28 d in milk treatment effects no longer existed. Overall, feeding 25-OH vitamin D with a negative DCAD diet increased vitamin D status of the cow and her newborn calf but had minimal effects on calcium status and did not have positive effects on the incidence of hypocalcemia.
The objective of this experiment was to determine the performance and digestibility response of lactating dairy cows fed a reduced-starch diet containing a commercial amylase product. Treatments consisted of a normal-starch total mixed ration (NS-), a reduced-starch total mixed ration (RS-), and a reduced-starch total mixed ration with exogenous amylase (RS+) added to the concentrate. Treatments were assigned according to a replicated 3 × 3 Latin square design with 28-d periods. Twenty-three cows completed the study. Starch concentrations in NS-, RS-, and RS+ total mixed rations were 27.7, 23.5, and 22.7%, respectively. Effects of treatment on intake, milk production, milk composition, and total-tract apparent nutrient digestibility were evaluated during the last week of each period. Effects of amylase on in vitro starch digestibility of the NS- and RS- grain mixes were also measured. We hypothesized that the reduction in dietary starch in the RS- ration would decrease diet digestibility and limit milk production compared with NS- due to a decrease in available energy, and that RS+ would alleviate some of this decrease by increasing nutrient digestibility. Contrary to this hypothesis, the RS- diet did not affect intake or milk production relative to the NS- diet, except for increased milk urea nitrogen and a tendency for a decrease in milk protein yield. This lack of response is attributed to both low milk fat concentrations across treatments and greater than predicted dietary energy content preventing the energy deficit that was intended to occur with the reduced-starch rations. Cows fed the RS+ ration had the lowest production performance, with reduced milk, fat-corrected milk, protein, and lactose yields relative to cows fed NS-. Cows fed RS+ also had reduced lactose yield and tended to have reduced milk and fat-corrected milk relative to cows fed RS-. Despite the negative effects of the RS+ treatment on performance, exogenous amylase did increase both in vitro and in vivo measurements of digestibility. Although amylase increased nutrient digestibility, this did not translate into improved milk performance, likely due to the relatively high energy content of experimental diets compared with cow requirements.
SummaryExogenous amylase, sucrose, or a combination was used in diets with reduced starch content. The trial was performed in 48 lactating Holstein cows, and milk yield, milk composition, and dry matter intake were measured. Treatments did not affect production traits, but with slightly decreased feed intake and slightly greater milk production in amylase-fed cows, the calculated value of amylase in this study was $0.37/cow per day.
A fluorescence microscope was used for visualization of the anticaging effect of a commercial xylanase on milled wheat, microtome cuts of wheat grains, and digesta samples obtained from piglets 1 or 4 h after feeding a wheat‐based diet (wheat 490 g/kg of diet, barley 100 g/kg of diet, and oats 100 g/kg of diet). Both starchy endosperm and aleurone cell walls were shown to be broken down by Ronozyme WX commercial xylanase. Data obtained by fluorescence microscopy was supplemented with measurements of starch and xylose released as a result of degradation of nonstarch polysaccharides by the xylanase. The results visualize and provide evidence that Ronozyme WX commercial xylanase can overcome the so‐called cage effect. This release of nutrients from their encapsulation in cereal cell wall structures has positive impact on nutrient digestibility and partially explains the positive effect of xylanase supplementation on livestock performance.
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