Rumen-protected choline reduces hepatic lipidosis by increasing hepatic triacylglycerol-rich lipoprotein secretion in dairy cows.

Objectives were to determine the effects of supplementing rumen-protected choline (RPC) on hepatic composition and secretion of triacylglycerol-rich lipoprotein when cows were subjected to feed restriction to develop fatty liver. It was hypothesized that RPC reduces hepatic triacylglycerol by enhancing secretion of hepatic lipoprotein. Pregnant, nonlactating parous Holstein cows (n = 33) at mean (± standard deviation) 234 ± 2.2 d of gestation were blocked by body condition (3.79 ± 0.49) and assigned to receive 0 g/d (CON), 25.8 g/d choline ion from a RPC product containing 28.8% choline chloride (CC; treatment L25.8), or 25.8 g/d of choline ion from a RPC product containing 60.0% CC (H25.8). Cows were fed for ad libitum intake for the first 5 d and restricted to 41% of the net energy for lactation required for maintenance and pregnancy from d 6 to 13. Intake of metabolizable methionine was maintained at 18 g/d during feed restriction by supplying rumen-protected methionine. Hepatic tissue was sampled on d 6 and 13 and analyzed for triacylglycerol and glycogen, and mRNA expression of hepatic tissue was investigated. On d 14, cows were not fed and received a 10% solution of tyloxapol intravenously at 120 mg/kg of body weight to block hydrolysis of triacylglycerols in very low density lipoprotein (VLDL). Blood was sampled sequentially for 720 min and analyzed for concentration of triacylglycerol and total cholesterol. Lymph was sampled 6 h after tyloxapol infusion, and analyzed for concentrations of fatty acids, ß-hydroxybutyrate, glucose, triacylglycerol, and total cholesterol. A sample of serum collected at 720 min after tyloxapol was assayed for the metabolome composition. The area under the curve (AUC) of serum triacylglycerol, VLDL cholesterol, and total cholesterol were calculated. Orthogonal contrasts evaluated the effect of supplementing RPC (CON vs. [1/2 L25.8 + 1/2 H25.8]) and source of RPC (L25.8 vs. H25.8). Least squares means and standard errors of the means are presented in sequence as CON, L25.8, H25.8. During feed restriction, supplementation of RPC reduced hepatic triacylglycerol (9.0 vs. 4.1 vs. 4.5 ± 0.6%) and increased glycogen contents (1.9 vs. 3.5 vs. 4.1 ± 0.2%). Similarly, supplementation of RPC increased the expression of transcripts involved in the synthesis and assembly of lipoproteins (MTTP), cellular autophagy (ATG3), and inflammation (TNFA), and reduced the expression of transcripts associated with mitochondrial oxidation of fatty acids (HADHA, MLYCD) and stabilization of lipid droplets (PLIN2). After infusion of tyloxapol, RPC increased the AUC for serum triacylglycerol (21,741 vs. 32,323 vs. 28,699 ± 3,706 mg/dL × min) and VLDL cholesterol (4,348 vs. 6,465 vs. 5,740 ± 741 mg/dL × min) but tended to reduce the concentrations of triacylglycerol in lymph (16.7 vs. 13.8 vs. 11.9 ± 1.9 mg/dL). Feeding RPC tended to increase the concentrations of 89 metabolites in serum, after adjusting for false discovery, including 3 acylcarnitines, 1 AA-related metabolite, 11 bile acids, 1 ceramide, 6 diacylglycerols, 2 dihydroceramides, 1 glycerophospholipid, and 64 triacylglycerols compared with CON. Feeding 25.8 g/d of choline ion as RPC mediated increased hepatic triacylglycerol secretion to promote lipotropic effects that reduced hepatic lipidosis in dairy cows.

Effect of source and amount of rumen-protected choline on hepatic metabolism during induction of fatty liver in dairy cows.

Objectives were to determine the effect of supplementing increased amounts of rumen-protected choline (RPC) from sources with low (L, 28.8%) or high (H, 60.0%) concentration of choline chloride on hepatic metabolism when cows were subjected to feed restriction to develop fatty liver. It was hypothesized that increased supplementation of RPC reduces hepatic triacylglycerol and enhances glycogen concentrations. Pregnant, nonlactating multiparous Holstein cows (n = 110) at mean (± standard deviation) 232 ± 3.9 d of gestation were blocked by body condition (4.01 ± 0.52) and assigned to receive 0 (CON), 12.9 (L12.9 or H12.9), or 25.8 (L25.8 or H25.8) g/d of choline ion. Cows were fed for ad libitum intake on d 1 to 5 and restricted to 50% of the NEL required for maintenance and pregnancy from d 6 to 13. Intake of metabolizable methionine was maintained at 19 g/d during the feed restriction period by supplying rumen-protected methionine. Hepatic tissue was sampled on d 6 and 13 and analyzed for triacylglycerol, glycogen, and mRNA expression of genes involved in choline, glucose, and fatty acids metabolism, cell signaling, inflammation, autophagy, lipid droplet dynamics, lipophagy, and endoplasmic reticulum stress response. Blood was sampled and analyzed for concentrations of fatty acids, ß-hydroxybutyrate (BHB), glucose, triacylglycerol, total cholesterol, and haptoglobin. Orthogonal contrasts evaluated the effect of supplementing RPC [CON vs. (1/4·L12.9 + 1/4·L25.8 + 1/4·H12.9 + 1/4·H25.8)], source of RPC [(1/2·L12.9 + 1/2·L25.8) vs. (1/2·H12.9 + 1/2·H25.8)], amount of RPC [(1/2·L12.9 + 1/2·H12.9) vs. (1/2·L25.8 + 1/2·H25.8)], and interaction between source and amount [(1/2·L12.9 + 1/2·H25.8) vs. (1/2·H12.9 + 1/2·L25.8)]. Least squares means and standard error of the means are presented in sequence as CON, L12.9, L25.8, H12.9, H25.8. Supplementation of RPC reduced hepatic triacylglycerol (9.3 vs. 6.6 vs. 5.1 vs. 6.6 vs. 6.0 ± 0.6% as-is) and increased glycogen contents (1.8 vs. 2.6 vs. 3.6 vs. 3.1 vs. 4.1 ± 0.2% as-is) on d 13 of the experiment. Feeding RPC reduced serum haptoglobin (136.6 vs. 85.6 vs. 80.6 vs. 82.8 vs. 81.2 ± 4.6 µg/mL) during the feed restriction period; however, blood concentrations of fatty acids, BHB, glucose, triacylglycerol, and total cholesterol did not differ among treatments. During feed restriction, supplementation of RPC enhanced the mRNA expression of genes related to choline metabolism (BHMT), uptake of fatty acids (CD36), and autophagy (ATG3), and reduced the expression of a transcript associated with endoplasmic reticulum stress response (ERN1). An increase in the amount of choline ion from 12.9 to 25.8 g/d enhanced the mRNA expression of genes associated with synthesis and assembly of lipoproteins (APOB100), and inflammation (TNFA), whereas it reduced the expression of genes linked to gluconeogenesis (PC), oxidation of fatty acids (ACADM, MMUT), ketogenesis (ACAT1), and synthesis of antioxidants (SOD1) on d 13 of the experiment. Feeding RPC, independent of the product used, promoted lipotropic effects that reduced hepatic lipidosis in dairy cows.

Induced endometritis in early lactation compromises production and reproduction in dairy cows.

Objectives of this experiment were to study the effect of infusing utero-pathogenic bacteria to induce endometrial inflammation on productive performance in early lactation and subsequent reproduction. Although endometritis is associated with perturbed reproduction, numerous factors may contribute to the observed association. It was hypothesized that induced endometrial inflammation, resulting in localized and systemic inflammatory responses, compromises production and reproduction. Holstein cows without clinical disease and with less than 18% polymorphonuclear leukocytes (PMN) in endometrial cytology on d 31 ± 3 postpartum had their estrous cycle synchronized. Cows were blocked by parity and genomic breeding value for cow conception rate and, within block, assigned randomly to remain as untreated controls (CON; n = 37) or to receive an intrauterine infusion of 5.19 × 108 cfu Escherichia coli and 4.34 × 108 cfu Trueperella pyogenes during the luteal phase to induce endometrial inflammation (INF; n = 48). Endometrial cytology was taken on d 2 and 7 after treatment to evaluate the proportion of PMN. Rectal temperature, dry matter intake, and yields of milk and components were measured in the first 7 d after treatment. Blood serum was analyzed for concentration of haptoglobin. Leukocytes were isolated from blood on d 2 and 7 after treatment and on d 19 after artificial insemination (AI) and mRNA was quantified for a select group of genes. Cows received AI and reproduction was followed for 300 d postpartum. Bacterial infusion induced endometrial inflammation with increased proportions of PMN in the endometrial cytology on d 2 (4.4 ± 0.7 vs. 26.3 ± 2.8%) and 7 (10.9 ± 1.7 vs. 17.4 ± 2.1%) after treatment, resulting in increased mean prevalence of subclinical endometritis (>10% PMN; 23.3 ± 6.3 vs. 80.9 ± 5.1%). Rectal temperature did not differ between CON and INF, but the concentration of haptoglobin in serum tended to increase in INF compared with CON (113 ± 14 vs. 150 ± 16 µg/mL). Induced endometrial inflammation reduced yields of milk (44.9 ± 0.8 vs. 41.6 ± 0.8 kg/d), protein (1.19 ± 0.03 vs. 1.12 ± 0.03 kg/d), and lactose (2.17 ± 0.04 vs. 2.03 ± 0.04 kg/d) and tended to reduce dry matter intake (20.7 ± 0.5 vs. 19.4 ± 0.6 kg/d) in the first 7 d after treatment. Indeed, the reduction in milk yield lasted 4 wk. However, treatment did not affect yields of energy-corrected milk or fat because treatment with INF increased the concentration of fat in milk (3.54 ± 0.10 vs. 3.84 ± 0.10%). Induced endometrial inflammation reduced pregnancy per AI at all inseminations (33.4 ± 5.1 vs. 21.6 ± 3.7%) and the hazard of pregnancy (0.61; 95% CI = 0.36-1.04), which extended the median days open by 24 d. Blood leukocytes from INF cows had increased mRNA expression of the pro-inflammatory gene IL1B on d 2 and 7 after treatment, but reduced expression of the IFN-stimulated genes ISG15 and MX2 on d 19 after AI. Induced endometrial inflammation depressed production and caused long-term negative effects on reproduction in lactating dairy cows.

Effect of source and amount of vitamin D on serum concentrations and retention of calcium, magnesium, and phosphorus in dairy cows.

The objectives of the experiment were to determine the effects of supplementing 2 amounts of 25-hydroxyvitamin D3 (calcidiol; CAL) compared with equal amounts of vitamin D3 (cholecalciferol; CHOL) on serum concentrations, absorptions, and retentions of Ca, Mg, and P in periparturient dairy cows. One hundred seventy-seven (133 parous and 44 nulliparous) pregnant Holstein cows were enrolled in the experiment. Cows were blocked by parity and previous lactation milk yield (parous) or genetic merit for energy-corrected milk yield (nulliparous) and assigned randomly to receive 1 or 3 mg/d of CAL or CHOL in a 2 × 2 factorial arrangement of treatments. Treatments were provided to individual cows as a top-dress to the prepartum diet from 250 d gestation until parturition. The prepartum diet had a dietary cation-anion difference of -128 mEq/kg of dry matter. All cows were fed a common postpartum diet containing 46 µg of vitamin D3/kg of dry matter without further supplementation of treatments. Concentrations of vitamin D metabolites, Ca, Mg, and P in serum were measured pre- and postpartum, in addition to total-tract digestibility and urinary excretion of Ca, Mg, and P in the prepartum period. Feeding 3 mg compared with 1 mg of CAL increased serum 25-hydroxyvitamin D3 (CAL1 = 94 vs. CAL3 = 173 ± 3 ng/mL). In comparison, the increment in serum 25-hydroxyvitamin D3 from feeding 3 mg compared with 1 mg of CHOL was small (CHOL1 = 58 vs. CHOL3 = 64 ± 3 ng/mL). Feeding CAL increased prepartum concentration of P in serum compared with CHOL (CHOL = 1.87 vs. CAL = 2.01 ± 0.02 mM), regardless of the amount fed, but neither source nor amount affected prepartum Ca or Mg in serum. Feeding CAL increased serum Ca and P for the first 11 d postpartum compared with CHOL (CHOL = 2.12 vs. CAL = 2.16 ± 0.01 mM serum Ca; CHOL = 1.70 vs. CAL = 1.78 ± 0.02 mM serum P) but the amount of vitamin D did not affect postpartum concentrations of Ca, Mg, and P in serum. Feeding CAL increased prepartum apparent digestibility of Ca compared with CHOL (CHOL = 26.6 vs. CAL = 33.5 ± 2.8%) but treatments did not affect Ca retention prepartum. Neither source nor amount of vitamin D affected Mg and P apparent digestibility, but CAL decreased the concentration of P excreted in urine during the prepartum period (CHOL = 1.8 vs. CAL = 0.8 ± 0.3 g/d). Calcidiol tended to increase the amount of Ca secreted in colostrum (CHOL = 9.1 vs. CAL = 11.2 ± 0.9 g/d) and Ca excreted in urine postpartum (CHOL = 0.4 vs. CAL = 0.6 ± 0.1 g/d) compared with CHOL. Collectively, feeding CAL at 1 or 3 mg/d compared with CHOL in the last 24 d of gestation is an effective way to increase periparturient serum P concentration and postpartum serum Ca of dairy cows fed a prepartum diet with negative DCAD.

Effect of prepartum source and amount of vitamin D supplementation on lactation performance of dairy cows.

The objectives of this experiment were to determine the effects of supplementing 25-hydroxyvitamin D3 (calcidiol, CAL) compared with vitamin D3 (cholecalciferol, CHOL) at 1 or 3 mg/d in late gestation on production outcomes of dairy cows. One hundred thirty-three parous and 44 nulliparous pregnant Holstein cows were enrolled in the experiment. Cows were blocked by parity and previous lactation milk yield (parous) or genetic merit (nulliparous) and assigned randomly to receive 1 or 3 mg/d of CAL or CHOL in a 2 × 2 factorial arrangement of treatments (CAL1, CAL3, CHOL1, and CHOL3). Treatments were provided to individual cows as a top-dress to the prepartum diet from 250 d in gestation until parturition. The prepartum diet had a dietary cation-anion difference of -128 mEq/kg of dry matter. Production and disease were evaluated for the first 42 d in milk, and reproduction was evaluated to 300 d in milk. Incidence of postpartum diseases did not differ among treatments. Feeding CAL compared with CHOL increased yields of colostrum and colostrum fat, protein, and total solids, resulting in an increased amount of net energy for lactation secreted as colostrum (CHOL = 7.0 vs. CAL = 9.0 ± 0.7 Mcal). An interaction between source and amount was observed for milk yield: CAL3 increased milk yield compared with CHOL3 (CHOL3 = 34.1 vs. CAL3 = 38.7 ± 1.4 kg/d) but milk yield did not differ between CAL1 and CHOL1 (CHOL1 = 36.9 vs. CAL1 = 36.4 ± 1.4 kg/d). Concentrations of serum calcidiol on day of calving and average serum Ca from d 2 to 11 postpartum were positively associated with milk yield in the first 42 d in milk. Interactions between source and amount of vitamin D were also observed for pregnancy after first AI: the percentage of cows receiving CHOL1 and CAL3 that became pregnant was smaller than that of cows receiving CHOL3 and CAL1. However, pregnancy per AI and pregnancy by 300 d in milk did not differ among treatments. Overall, CAL3 increased milk yield compared with CHOL3, whereas in cows fed 1 mg/d (CAL1 and CHOL1), the source of vitamin D generally had no effect. The effect of CAL3 may be explained in part by serum CAL concentrations and postpartum serum Ca, which were associated with milk yield.

Prepartum level of dietary cation-anion difference fed to nulliparous cows: Acid-base balance, mineral metabolism, and health responses.

Objectives were to determine the effects of 3 different levels of dietary cation-anion difference (DCAD) fed during the last 22 d of gestation to pregnant nulliparous cows on pre- and postpartum acid-base balance, mineral metabolism, and health responses. In all, 132 pregnant nulliparous Holstein cows were enrolled at 250 (248-253) d of gestation, blocked by genomic merit of energy-corrected milk yield, and assigned randomly to diets varying in DCAD: +200 (P200, n = 43), -50 (N50, n = 45), or -150 (N150, n = 44) mEq/kg of dry matter. Dietary treatments were fed until calving, after which cows received the same lactation diet for the first 100 d postpartum. Urine and blood were sampled throughout the prepartum period and in the first weeks postpartum, and urine was assessed for pH, whereas blood was analyzed for gases, measures of acid-base balance, minerals, and metabolites. Calcium (Ca) and magnesium (Mg) retention and phosphorus (P) digestibility were evaluated in the last week of gestation and first week of lactation. Incidence of diseases was evaluated for the first 100 d postpartum. Data are presented in sequence as P200, N50, N150 (LSM ± SEM). Reducing the DCAD reduced urine (8.17 vs. 6.50 vs. 5.51 ± 0.11) and blood pH (7.442 vs. 7.431 vs. 7.410 ± 0.004) and induced a state of compensated metabolic acidosis with a reduction in blood HCO3- (28.4 vs. 26.7 vs. 24.9 ± 0.3 mM) and partial pressure of CO2 (41.8 vs. 40.1 vs. 39.1 ± 0.4 mmHg) prepartum. Reducing the DCAD linearly increased blood ionized Ca (iCa; 1.224 vs. 1.243 vs. 1.259 ± 0.008 mM) and serum total Ca (tCa; 2.50 vs. 2.53 vs. 2.56 ± 0.02 mM) prepartum, blood iCa on the day of calving, and serum Mg in the first days postpartum. Reducing the DCAD linearly increased the apparent absorption of Ca (12.9 vs. 19.0 vs. 20.9 ± 1.4 g/d) and Mg (7.0 vs. 9.9 vs. 10.4 ± 1.4 g/d) prepartum, but apparent retention of both Ca (13.9 g/d) and Mg (3.4 g/d) did not differ with treatment. Treatment did not affect digestibility of P pre- or postpartum or retention of Ca or Mg postpartum. Treatment did not affect the incidence or prevalence of subclinical hypocalcemia, hepatic composition, or the prevalence of fatty liver. Reducing the DCAD had a quadratic effect on incidence of fever (46.5 vs. 17.6 vs. 33.9 ± 7.0%), uterine diseases (36.3 vs. 25.6 vs. 46.0 ± 7.3%), and morbidity (41.4 vs. 28.1 vs. 55.6 ± 7.3%). Feeding a diet with -50 mEq/kg of dry matter promoted moderate changes in acid-base balance, altered mineral metabolism, and benefited health of nulliparous cows; however, further reducing the DCAD to -150 mEq/kg negated the benefits to health.

Prepartum level of dietary cation-anion difference fed to nulliparous cows: Lactation and reproductive responses.

Objectives were to determine the effects of 3 levels of dietary cation-anion difference (DCAD) fed prepartum to nulliparous cows on productive and reproductive performance. We enrolled 132 pregnant nulliparous Holstein cows at 250 (248-253) d of gestation in a randomized block design. Cows were blocked by genomic merit of energy-corrected milk yield and assigned randomly to diets varying in DCAD, +200 (P200; n = 43), -50 (N50; n = 45), or -150 (N150; n = 44) mEq/kg of dry matter (DM). Dietary treatments were fed during the last 22 d of gestation and, after calving, postpartum cows received the same lactation diet. Productive performance was evaluated for the first 14 wk of lactation, and reproduction was assessed until 305 d postpartum. Intake of DM prepartum decreased linearly (results presented in sequence as least squares means ± standard error of the mean, P200 vs. N50 vs. N150) with a reduction in DCAD (9.0 vs. 8.9 vs. 8.4 ± 0.1 kg/d), which resulted in linear decreases in net energy balance (0.34 vs. 0.20 vs. -0.36 ± 0.20 Mcal/d), body weight change (1.1 vs. 0.8 vs. 0.3 ± 0.1 kg/d), and mean body weight (652 vs. 649 vs. 643 ± 2 kg) prepartum. Treatment did not affect yield of colostrum (6.3 vs. 5.8 vs. 5.1 ± 0.6 kg) or the contents or yields of fat, protein, lactose, IgG, Ca, or Mg in colostrum. Intake of DM (19.4 vs. 19.2 vs. 19.0 ± 0.2 kg/d), yields of milk (36.6 vs. 36.7 vs. 35.8 ± 0.6 kg/d) or energy-corrected milk (36.7 vs. 36.3 vs. 35.9 ± 0.5 kg/d), feed efficiency (1.93 vs. 1.92 vs. 1.93 ± 0.03 kg of energy-corrected milk per kilogram of DM intake), and content and yield of milk components did not differ among treatments during the first 14 wk of lactation. Prepartum DCAD did not affect the cumulative milk yield by 305 d of lactation (9,653 vs. 10,005 vs. 9,918 ± 196 kg). Of the 132 cows, 40 P200, 45 N50, and 43 N150 received at least 1 artificial insemination (AI), and treatment did not affect pregnancy per AI at first (32.5 vs. 35.6 vs. 37.2%) or all AI (30.6 vs. 33.9 vs. 40.2%), although reducing the DCAD increased the proportion of cows pregnant by 305 d postpartum (76.7 vs. 88.9 vs. 93.2%) without altering the rate of pregnancy. Collectively, manipulating the DCAD of prepartum diets, from +200 to -150 mEq/kg of DM, fed to late gestation nulliparous cows did not affect subsequent lactation productive performance, but may have provided some benefit to reproduction, which warrants further confirmation.

Effect of source and amount of vitamin D on function and mRNA expression in immune cells in dairy cows.

Objectives were to determine the effect of supplementing 2 sources of vitamin D, cholecalciferol (CH) or calcidiol (CA), at 1 (1mg) or 3 mg/d (3mg) prepartum on concentrations of vitamin D metabolites in plasma, measures of innate immune function, and leukocyte mRNA expression. Parous Holstein cows (n = 99) were assigned to a daily treatment administered as top-dress containing either 1 or 3 mg of CH (CH1 or CH3) or of CA (CA1 or CA3) from 250 d of gestation until calving. Plasma concentrations of vitamin D, immune cell population in blood, cell adhesion markers, and granulocyte phagocytosis and oxidative burst were evaluated pre- and postpartum. The mRNA expression in leukocytes was determined at 270 d of gestation and 3 d postpartum for genes involved in cell migration, pathogen recognition receptors, cell signaling, cytokines, antimicrobial mechanisms, oxidative burst, and Ca and vitamin D metabolism. Concentrations of vitamin D3 increased in cows fed CH, whereas those of 25-hydroxyvitamin D3 increased in cows fed CA. Percentage of granulocytes from total leukocytes differed with amount of vitamin D pre- (1mg = 24.5 vs. 3mg = 37.9%) and postpartum (1mg = 22.0 vs. 3mg = 31.0%), thus shifting mononuclear cells in the opposite direction pre- (1mg = 75.5 vs. 3mg = 62.1%) and postpartum (1mg = 78.0 vs. 3mg = 69.0%). Granulocytes displaying phagocytosis (1mg = 69.0 vs. 3mg = 62.9%) and intensity of phagocytosis prepartum (1mg = 7.46 vs. 3mg = 7.28) tended to be less in cows fed 3mg compared with 1mg. During prepartum, CA increased mRNA expression of genes related to cell adhesion and migration (CD44, ICAM1, ITGAL, ITGB1, LGALS8, SELL), pathogen recognition receptor (NOD2, TLR2, TLR6), cell signaling (FOS, JUN, NFKB2), cytokine signaling (IL1B, IL1R1, IL1RN), antimicrobial mechanisms (CTSB, LYZ), and Ca metabolism (ATP2B1, STIM1, TRPV5) compared with CH. Similarly, postpartum, CA increased mRNA expression of genes related to cell adhesion and migration (CXCR2, SELL, TLN1), cell signaling (AKT2), cytokines (CCL2, IL1R1, ILRN), antimicrobial mechanisms (DEFB3), oxidative burst (RAC2), and calcium metabolism (CALM3) compared with CH. Feeding additional vitamin D in the last 3 wk of gestation changed the profile of blood leukocytes and attenuated granulocyte phagocytosis during the transition period, whereas supplementing CA prepartum increased mRNA expression of genes involved in immune cell function, including genes related to pathogen recognition and antimicrobial effects of leukocytes.

Effects of maternal level of dietary cation-anion difference fed to prepartum nulliparous cows on offspring acid-base balance, metabolism, and growth.

The objectives were to determine the effects of dietary cation-anion difference (DCAD) fed to pregnant cows during the last 22 d of gestation on offspring acid-base balance, metabolism, growth, and health preweaning. A total of 132 nulliparous Holstein cows were enrolled at 250 (248 to 253) d of gestation in a randomized block design. Cows were blocked by genomic merit of energy-corrected milk yield and assigned randomly to diets varying in DCAD: +200 (P200, n = 43), -50 (N50, n = 45), or -150 (N150, n = 44) mEq/kg of dry matter (DM). Newborn calves (15 males and 28 females in P200, 22 males and 23 females in N50, and 18 males and 26 females in N150) were followed for the first 7 or 56 d of age if males or females, respectively. Measures of acid-base balance and concentrations of minerals in blood were measured in all calves on d 0 before colostrum feeding, and on d 1, 3, and 7. Each calf was fed 3.78 L of colostrum from the respective treatment, and apparent efficiency of IgG absorption was determined. All calves were weighed at birth, and females were weighed again at 21, 42, and 56 d of age. Concentrations in serum of total calcium (tCa), total magnesium (tMg), and total phosphorus (tP) were measured up to 56 d of age; intakes of milk and starter grain DM were measured daily from 21 to 56 d of age; and incidence of disease was recorded for the first 56 d of age in females. Treatment did not affect acid-base balance measured in all calves. Calves were born with metabolic and respiratory acidosis, which reversed by 1 d of age. In the first 24 h after birth, blood pH increased from 7.215 to 7.421 and bicarbonate from 26.2 to 31.7 mM, whereas partial pressure of CO2 decreased from 64.1 to 48.7 mm of Hg in all treatments. Maternal DCAD did not affect colostrum IgG content fed to calves (P200 = 95.0 vs. N50 = 91.0 vs. N150 = 97.1 ± 4.1 g/L) or apparent efficiency of IgG absorption (P200 = 33.1 vs. N50 = 33.1 vs. N150 = 34.2 ± 1.9%). Males were born heavier than females, but maternal DCAD did not affect birth weight of all calves (P200 = 37.7 vs. N50 = 37.3 vs. N150 = 37.8 ± 0.7 kg) or daily weight gain in females in the first 56 d of life (P200 = 0.80 vs. N50 = 0.81 vs. N150 = 0.77 ± 0.03 kg/d). Treatment did not affect intake of milk (P200 = 1.11 vs. N50 = 1.04 vs. N150 = 1.19 ± 0.06 kg/d) or starter grain DM (P200 = 0.27 vs. N50 = 0.27 vs. N150 = 0.21 ± 0.06 kg/d), or measures of feed efficiency. Treatment did not affect concentrations of minerals in serum, morbidity, or age at morbidity. Manipulating the DCAD of pregnant nulliparous dams during late gestation did not affect offspring performance in the first 2 mo of age.

Days in the prepartum group are associated with subsequent performance in Holstein cows.

Our objective was to evaluate the association between days in the prepartum group (DPG) with performance and survival in Holstein cows. Data from 18,657 Holstein cow-lactations (6,993 nulliparous and 9,390 parous prepartum) were collected. Cows with a gestation length shorter than 256 d (n = 267) or longer than 296 d (n = 131) and cows that spent 0 DPG (n = 238) were removed, resulting in 18,021 cow-lactations. Data were collected for the first 300 d postpartum, and responses included milk yield, incidence of diseases by 90 d postpartum, reproduction, and survival. Days in the prepartum group were analyzed as a continuous variable, and regression coefficients were used to estimate the responses when cows spent 7, 28, or 42 DPG, representing cows with a short, moderate, or an extended time in the prepartum group, respectively. An interaction between DPG as a quadratic covariate and parity-diet was observed for milk yield by 300 d postpartum. Means were 9,331; 9,665; and 9,261 kg for 7, 28, or 42 DPG, respectively, in nulliparous cows, and 9,886; 10,939; and 10,117 kg for 7, 28, or 42 DPG, respectively, in parous cows. Also, the interaction between DPG and parity-diet affected retained placenta, metritis, mastitis, and morbidity. Morbidity affected 49.5, 52.9, and 59.5% of nulliparous and 49.7, 26.5, and 47.4% of parous cows that spent 7, 28, or 42 DPG, respectively. A linear association between DPG and pregnancy at first artificial insemination was observed with estimates of 37.0, 32.6, and 29.8% for 7, 28, and 42 DPG, respectively. On the other hand, a quadratic association was observed between DPG and the proportion of pregnant cows at 300 d postpartum, and estimates for 7, 28, and 42 DPG were, respectively, 71.7, 73.5, and 58.8%. A quadratic relationship was also observed for DPG and removal from the herd by 300 d postpartum, and estimates were 25.2, 22.9, and 34.4% for 7, 28, or 42 DPG, respectively. Associations between DPG with production, health, reproduction, and survival were detected, and they varied with parity-diet group. For several responses evaluated, a quadratic association was observed, which suggested that there was an optimal period for cows to spend in the prepartum group, and reduced or extended number of days were detrimental to performance.

Assessing feed efficiency in early and mid lactation and its associations with performance and health in Holstein cows.

Objectives were to evaluate the associations between residual dry matter (DM) intake (RFI) and residual N intake (RNI) in early lactation, from 1 to 5 wk postpartum, and in mid lactation, from 9 to 15 wk postpartum, and assess production performance and risk of diseases in cows according to RFI in mid lactation. Data from 4 experiments including 399 Holsteins cows were used in this study. Intakes of DM and N, yields of milk components, body weight, and body condition were evaluated daily or weekly for the first 105 d postpartum. Milk yield by 305 d postpartum was also measured. Incidence of disease was evaluated for the first 90 d postpartum and survival up to 300 d postpartum. Residual DM and N intake were calculated in early and mid lactation as the observed minus the predicted values, which were based on linear models that accounted for major energy or N sinks, including daily milk energy or N output, metabolic body weight, and daily body energy or N changes, and adjusting for parity, season of calving, and treatment within experiment. Cows were ranked by RFI and RNI in mid lactation and categorized into quartiles (Q1 = smallest RFI, to Q4 = largest RFI). Increasing efficiency in mid lactation resulted in linear decreases in RFI (depicted from Q1 to Q4; -0.93, -0.05, -0.04, and 0.98 kg/d), DMI (16.0, 16.9, 17.3, and 18.4 kg/d), net energy for lactation (NEL) intake (26.8, 28.4, 29.0, and 30.8 Mcal/d), and NEL balance (-9.0, -8.1, -8.2, and -5.5 Mcal/d) during early lactation, but no differences were observed in body NEL or N changes or yield of energy-corrected milk in the first 5 wk of lactation. Residual DM intake in mid lactation was associated with RFI (Pearson r = 0.43, and Spearman ρ = 0.32) and RNI (r = 0.44, ρ = 0.36) in early lactation, and with RNI in mid lactation (r = 0.91, ρ = 0.84). Similarly, RNI in mid lactation was associated with RNI in early lactation (r = 0.42, ρ = 0.35). During the first 15 wk postpartum, more efficient cows in mid lactation consumed 3.5 kg/d less DM (Q1 = 19.3 vs. Q4 = 22.8 kg/d) and were more N efficient (Q1 = 31.6 vs. Q4 = 25.8%), at the same time that yields of milk (Q1 = 39.0 vs. Q4 = 39.4 kg/d), energy-corrected milk (Q1 = 38.6 vs. Q4 = 39.3 kg/d), and milk components did not differ compared with the quartile of least efficient cows. Furthermore, RFI in mid lactation was not associated with 305-d milk yield, incidence of diseases in the first 90 d postpartum, or survival by 300 d postpartum. Collectively, rankings of RFI and RNI are associated and repeatable across lactation stages. The most feed-efficient cows were also more N efficient in early and mid lactation. Phenotypic selection of RFI based on measurements in mid lactation is associated with improved efficiency without affecting production or health in dairy cows.

Duration and degree of diet-induced metabolic acidosis prepartum alter tissue responses to insulin in dairy cows.

The objective of this experiment was to determine the effects of altering the dietary cation-anion difference (DCAD) fed for the last 21 or 42 d of gestation on glucose metabolism and tissue insulin responsiveness. Ninety parous Holstein cows at 232 d of gestation were assigned randomly to dietary treatments with 2 levels of DCAD (-70 or -180 mEq/kg) fed for 2 durations (short: the last 21 d of gestation; long: the last 42 d of gestation). For the short treatments, a diet with +110 mEq/kg was fed from 232 to 254 d of gestation. Intravenous glucose tolerance tests (IVGTT) were performed at either 250 or 270 d of gestation by infusing 0.25 g of dextrose/kg of body weight within 1 min. The following day, cows underwent an insulin challenge (IC) and received 0.1 IU of insulin/kg of body weight intravenously. Blood was sampled at min -15, -5, and 0 to establish a baseline and from 5 to 180 min relative to infusions; plasma concentrations of glucose, insulin, and fatty acids were determined, and the respective areas under the curves (AUC) were calculated. Liver was sampled after the IVGTT, and adipose tissue was sampled after the IVGTT and IC for quantification of mRNA expression and protein abundance. Reducing the DCAD altered acid-base balance compatible with a compensated metabolic acidosis. At 250 d, reducing the DCAD increased the AUC for glucose and reduced that of insulin following the IVGTT, whereas during the IC, clearance rate decreased and time to half-life of insulin increased with reducing DCAD, resulting in a tendency to a larger AUC for fatty acids. At 270 d, quantitative insulin sensitivity check index and the revised quantitative insulin sensitivity check index were smaller in cows fed the acidogenic diets for the last 42 d of gestation compared with the last 21 d of gestation, thereby suggesting reduced insulin sensitivity. In addition, cows fed for the long duration tended to have greater AUC for glucose but smaller AUC for insulin following an IVGTT than those fed for the short duration, thereby suggesting reduced insulin release and glucose disposal. Treatments did not affect hepatic mRNA expression of G6PC, PCK1, PCK2, and PC or adipose tissue mRNA expression of ATGL, ACC, B2AR, HSL, and PLIN1. On the other hand, for proteins, reducing the DCAD linearly reduced abundance of rabbit anti-mouse protein kinase B (AKT) and tended to reduce rabbit anti-human phosphorylated (Ser-9) glycogen synthase kinase-3 ß (pGSK) and the pGSK:rabbit anti-human glycogen synthase kinase-3 ß (GSK) ratio in hepatic tissue, whereas a linear increase in rabbit anti-human hormone-sensitive lipase (HSL) and rabbit anti-mouse phosphorylated (Ser-660) hormone-sensitive lipase (pHSL) in adipose tissue was observed after the IVGTT at 250 d. Moreover, reducing the DCAD resulted in a linear reduction of AKT and tended to reduce rabbit anti-human acetyl-CoA carboxylase (ACC) but increased pHSL linearly in adipose tissue after an IC at 250 d. Cows fed acidogenic diets for a short duration tended to have less pHSL in adipose tissue than those fed for a long duration after an IVGTT at 270 d. Associations were observed between blood pH and mRNA and protein abundance in hepatic and adipose tissues. Diet-induced metabolic acidosis altered insulin release and insulin signaling, resulting in a shift in adipose tissue metabolism that would favor lipolysis over lipogenesis.

Effects of injectable calcitriol on mineral metabolism and postpartum health and performance in dairy cows.

Objectives were to determine the effects of an injectable formulation of calcitriol on Ca concentration, risk of clinical diseases, and performance in dairy cows. Cows were blocked by lactation number (1 vs. >1) and calving sequence and, within block, assigned randomly within 6 h of calving to receive subcutaneously vehicle only (CON, n = 450) or 200 (CAL200, n = 450) or 300 µg of 1α,25-dihydroxyvitamin D3 (CAL300, n = 450). Cows were fed the same acidogenic diet prepartum. Blood was sampled before treatment administration and again during the first 11 d postpartum and analyzed for concentrations of ionized Ca (iCa), total Ca (tCa), Mg (tMg), and P (tP), ß-hydroxybutyrate, carboxylated osteocalcin (cOC), and undercarboxylated osteocalcin (uOC). Cows were evaluated for diseases in the first 60 d postpartum. Reproduction and survival were monitored for the first 300 d postpartum. Calcitriol increased concentration of blood iCa (CON = 1.12 vs. CAL200 = 1.23 vs. CAL300 = 1.27 mM), plasma tCa (CON = 2.29 vs. CAL200 = 2.44 vs. CAL300 = 2.46 mM), and plasma tP (CON = 1.72 vs. CAL200 = 2.21 vs. CAL300 = 2.28 mM), and differences were observed during the first 5 d postpartum for iCa and tCa, and the first 7 d postpartum for tP. Concentrations of tMg were lower in calcitriol-treated cows than in CON cows (CON = 0.81 vs. CAL200 = 0.78 vs. CAL300 = 0.75 mM), and differences were observed during the first 5 d postpartum. Calcitriol increased plasma concentrations of cOC (CON = 14.5 vs. CAL200 = 23.0 vs. CAL300 = 19.8 ng/mL) and uOC (CON = 1.6 vs. CAL200 = 3.4 vs. CAL300 = 2.6 ng/mL). Prevalence of subclinical hypocalcemia was less in calcitriol-treated cows (CON = 19.0 vs. CAL200 = 4.7 vs. CAL300 = 9.3%); however, benefits on health were only observed in overconditioned cows (n = 270/1,350). Calcitriol reduced incidence of retained placenta (CON = 14.3 vs. CAL200 = 5.1 vs. CAL300 = 5.9%), puerperal metritis (CON = 12.7 vs. CAL200 = 6.1 vs. CAL300 = 2.5%), and morbidity (CON = 72.1 vs. CAL200 = 57.4 vs. CAL300 = 56.9%) in cows with BCS greater than 3.50, but no benefit on health was observed in cows with BCS equal to or less than 3.50 at parturition. Milk yield did not differ among treatments. Pregnancy at first AI did not differ, but pregnancy rate after the first AI was slower for calcitriol-treated cows because of reduced insemination rate and pregnancy per AI. We found that CAL200 reduced death but increased culling in cows without calving problems. Collectively, results indicate that treatment with calcitriol at parturition was effective in improving concentrations of iCa, tCa, and tP, which reduced the risk of hypocalcemia. Pregnancy rate was reduced by calcitriol treatment, and benefits on health performance were limited to overconditioned cows. Thus, treatment of all cows is not supported, and proper identification of cohorts of cows that benefit from postpartum interventions that increase blood calcitriol or calcium is needed.

Effect of duration of exposure to diets differing in dietary cation-anion difference on Ca metabolism after a parathyroid hormone challenge in dairy cows.

Objectives of the experiment were to determine the length of exposure to an acidogenic diet that would elicit changes in acid-base balance, mineral digestion, and response to parathyroid hormone (PTH)-induced changes in blood Ca and vitamin D3 in prepartum dairy cows. Nonlactating parous Holstein cows (n = 20) at 242 d of gestation were blocked by lactation (1 or >1) and pretreatment dry matter (DM) intake and, within block, they were randomly assigned to a diet with a dietary cation-anion difference (DCAD) of +200 mEq/kg of DM (DCAD +200) or an acidogenic diet with -150 mEq/kg of DM (DCAD -150). Water and DM intake were measured and blood was sampled daily. Urine was sampled every 3 h for 36 h, and then daily. During PTH challenges on d 3, 8, and 13, cows received i.v. PTH 1-34 fragment at 0.05 µg/kg of body weight every 20 min for 9 h to mimic the pulsatile release of endogenous PTH. Blood was sampled at 0 h, and hourly thereafter until 10 h, and at 12, 18, 24, 36, and 48 h relative to each challenge. Acid-base measures and concentrations of ionized Ca (iCa) in whole blood, and total Ca, Mg, P, and vitamin D metabolites in plasma were evaluated. On d 2 and 7, Ca, Mg, and P balances were evaluated. Cows fed DCAD -150 had smaller blood pH (7.431 vs. 7.389) and HCO3- (27.4 vs. 22.8 mM) compared with DCAD +200, and metabolic acidosis in DCAD -150 was observed 24 h after dietary treatments started. Concentrations of iCa begin to increase 24 h after feeding the acidogenic diet, and it was greater in DCAD -150 compared with DCAD +200 by 3 d in the experiment (1.23 vs. 1.26 mM). During the PTH challenges, cows fed DCAD -150 had greater concentration of iCa and area under the curve for iCa than those fed DCAD +200 (48.2 vs. 50.7 mmol/L × hour), and there was no interaction between treatment and challenge day. Concentration of 1,25-dihydroxyvitamin D3 in plasma did not differ during the PTH challenge, but change in 1,25-dihydroxyvitamin D3 relative to h 0 of the challenge was smaller in cows fed DCAD -150 than cows fed DCAD +200 (44.1 vs. 32.9 pg/mL). Urinary loss of Ca was greater in cows fed DCAD -150 compared with DCAD +200 (1.8 vs. 10.8 g/d); however, because digestibility of Ca increased in cows fed DCAD -150 (19.7 vs. 36.6%), the amount of Ca retained did not differ between treatments. Diet-induced metabolic acidosis was observed by 24 h after dietary treatment started, resulting in increases in concentration of iCa in blood observed between 1 and 3 d. Collectively, present results indicate that tissue responsiveness to PTH and changes in blood concentrations of iCa and digestibility of Ca are elicited within 3 d of exposure to an acidogenic diet. The increased apparent digestibility of Ca compensated for the increased urinary loss of Ca resulting in similar Ca retention.

Prostaglandin F2α influences pre-ovulatory follicle characteristics and pregnancy per AI in anovular dairy cows.

Objectives were to determine the effects of a dose of PGF2α administered 2 days before timed artificial insemination (AI) on LH pulsatility, characteristics of the pre-ovulatory follicle, and pregnancy per artificial insemination (P/AI) in anovular dairy cows, particularly in cows not subjected to hyperthermia. In experiment 1, 2,011 lactating Holstein cows had ovaries scanned by ultrasound to determine corpus luteum (CL) presence and only those without a CL in two consecutive exams were enrolled (n = 437). Cows had the estrous cycle synchronized with an estradiol-progesterone based protocol starting on experiment Day -11 and timed AI on Day 0. Cows were assigned randomly to receive a single dose of 25 mg of PGF2α as dinoprost on Day -4 (1PGF, n = 222) or two doses of 25 mg each of PGF2α, one on Day -4 and one on Day -2 (2PGF, n = 215). Rectal temperatures were evaluated on the day of AI and 7 days later and cows were classified as being normothermic (<39.1 °C) or hyperthermic (≥39.1 °C). Ovulatory responses and P/AI were determined. In experiment 2, cows with regressed CL were exposed to low concentrations of progesterone and then randomly assigned to the same estrous synchronization protocol and treatments, 1PGF (n = 28) and 2PGF (n = 28). Blood was sampled and analyzed for concentrations of progesterone, and for concentrations of LH and 13,14-dihydro-15-keto-PGF2α metabolite (PGFM) every 15 min starting 1 h before to 6 h after treatments and then every 2 h from 12 to 59 h after treatments. The pre-ovulatory follicle was aspirated 44 h after treatments and concentrations of estradiol quantified. In experiment 1, treatment of anovular cows with a second dose of PGF2α increased P/AI in normothermic cows (19.8 [18/91] vs. 38.8% [31/80]), but not in hyperthermic cows. Synchronization was not affected by treatment, but it was greater for normothermic than hyperthermic cows (87.1 [149/171] vs. 77.8% [207/266]). When only synchronized cows were evaluated, the same responses were observed; treatment with 2PGF increased P/AI compared with 1PGF in normothermic cows (23.1 [18/78] vs. 43.7% [31/71]), but not in hyperthermic cows. In experiment 2, administration of 25 mg of dinoprost in 2PGF resulted in concentrations of PGFM 26-fold greater than 1PGF in the first 6 h after treatment (48 vs. 1,242 pg/mL). Cows receiving 2PGF had smaller basal LH concentration (0.57 vs. 0.46 ng/mL) and less frequent LH pulses (4.5 vs. 3.9 pulses/6 h), but duration of the LH surge was longer for 2PGF than 1PGF (13.1 vs. 15.5 h). Treatment with 2PGF increased the diameter and volume of the pre-ovulatory follicle, and concentration of estradiol (115 vs. 262 ng/mL) and total follicular estradiol content (124 vs. 505 ng) compared with 1PGF. Collectively, these results suggest that PGF2α has a role in fertility of anovular cows that is unrelated to its luteolytic effect.

Effect of dietary cation-anion difference on acid-base status and dry matter intake in dry pregnant cows.

The objective was to determine if the reduction in dry matter (DM) intake of acidogenic diets is mediated by inclusion of acidogenic products, content of salts containing Cl, or changes in acid-base status. The hypothesis was that a decrease in intake is mediated by metabolic acidosis. Ten primigravid Holstein cows at 148 ± 8 d of gestation were used in a duplicated 5 × 5 Latin square design. The dietary cation-anion difference (DCAD) of diets and acid-base status of cows were manipulated by incorporating an acidogenic product or by adding salts containing Cl, Na, and K to the diets. Treatments were a base diet (T1; 1.42% K, 0.04% Na, 0.26% Cl; DCAD = 196 mEq/kg); the base diet with added 1% NaCl and 1% KCl (T2; 1.83% K, 0.42% Na, 1.23% Cl; DCAD = 194 mEq/kg); the base diet with added 7.5% acidogenic product, 1.5% NaHCO3, and 1% K2CO3 (T3; 1.71% K, 0.54% Na, 0.89% Cl; DCAD = 192 mEq/kg); the base diet with added 7.5% acidogenic product (T4; 1.29% K, 0.13% Na, 0.91% Cl; DCAD = -114 mEq/kg); and the base diet with 7.5% acidogenic product, 1% NaCl, and 1% KCl (T5; 1.78% K, 0.53% Na, 2.03% Cl; DCAD = -113 mEq/kg). Periods lasted 14 d with the last 7 d used for data collection. Feeding behavior was evaluated for 12 h in the last 2 d of each period. Reducing the DCAD by feeding an acidogenic product reduced blood pH (T1 = 7.450 vs. T2 = 7.436 vs. T3 = 7.435 vs. T4 = 7.420 vs. T5 = 7.416) and induced a compensated metabolic acidosis with a reduction in bicarbonate, base excess, and partial pressure of CO2 in blood, and reduced pH and strong ion difference in urine. Reducing the DCAD reduced DM intake 0.6 kg/d (T1 = 10.3 vs. T4 = 9.7 kg/d), which was caused by the change in acid-base status (T2 + T3 = 10.2 vs. T4 + T5 = 9.6 kg/d) because counteracting the acidifying action of the acidogenic product by adding salts with strong cations to the diet prevented the decline in intake. The decline in intake caused by metabolic acidosis also was observed when adjusted for body weight (T2 + T3 = 1.75 vs. T4 + T5 = 1.66% BW). Altering the acid-base status with acidogenic diets reduced eating (T2 + T3 = 6.7 vs. T4 + T5 = 5.9 bouts/12 h) and chewing (T2 + T3 = 14.6 vs. T4 + T5 = 13.5 bouts/12 h) bouts, and extended meal duration (T2 + T3 = 19.8 vs. T4 + T5 = 22.0 min/meal) and intermeal interval (T2 + T3 = 92.0 vs. T4 + T5 = 107.7 min). Results indicate that reducing the DCAD induced a compensated metabolic acidosis and reduced DM intake, but correcting the metabolic acidosis prevented the decline in DM intake in dry cows. The decrease in DM intake in diets with negative DCAD was mediated by metabolic acidosis and not by addition of acidogenic product or salts containing Cl.

Effects of level of dietary cation-anion difference and duration of prepartum feeding on performance and metabolism of dairy cows.

The objectives were to evaluate the effects of feeding diets with 2 levels of negative dietary cation-anion differences (DCAD) during the last 42 or 21 d of gestation on performance and metabolism in dairy cows. The hypothesis was that extending feeding from 21 to 42 d and reducing the DCAD from -70 to -180 mEq/kg of dry matter (DM) would not be detrimental to performance. Holstein cows at 230 d of gestation were blocked by parity prepartum (48 entering their second lactation and 66 entering their third or greater lactation) and 305-d milk yield, and randomly assigned to 1 of 4 treatments arranged as a 2 × 2 factorial. The 2 levels of DCAD, -70 or -180 mEq/kg of DM, and 2 feeding durations, the last 21 d (short) or the last 42 d (long) prepartum resulted in 4 treatments, short -70 (n = 29), short -180 (n = 29), long -70 (n = 28) and long -180 (n = 28). Cows in the short treatments were fed a diet with DCAD of +110 mEq/kg of DM from -42 to -22 d relative to calving. After calving, cows were fed the same diet and production and disease incidence were evaluated for 42 d in milk, whereas reproduction and survival was evaluated for 305 d in milk. Blood was sampled pre- and postpartum for quantification of metabolites and minerals. Reducing the DCAD linearly decreased prepartum DM intake between -42 and -22 d relative to calving (+110 mEq/kg of DM = 11.5 vs. -70 mEq/kg of DM = 10.7 vs. -180 mEq/kg of DM = 10.2 ± 0.4), and a more acidogenic diet in the last 21 d of the dry period reduced intake by 1.1 kg/d (-70 mEq/kg of DM = 10.8 vs. -180 mEq/kg of DM = 9.7 ± 0.5 kg/d). Cows fed the -180 mEq/kg of DM diet had increased concentrations of ionized Ca in blood on the day of calving (-70 mEq/kg of DM = 1.063 vs. -180 mEq/kg of DM = 1.128 ± 0.020 mM). Extending the duration of feeding the diets with negative DCAD from 21 to 42 d reduced gestation length by 2 d (short = 277.2 vs. long = 275.3 d), milk yield by 2.5 kg/d (short = 40.4 vs. long = 37.9 ± 1.0 kg/d) and tended to increase days open because of reduced pregnancy per artificial insemination (short = 35.0 vs. long = 22.6%). Results suggest that increasing the duration of feeding diets with negative DCAD from 21 to 42 d prepartum might influence milk yield and reproduction of cows in the subsequent lactation, although yields of 3.5% fat- and energy-corrected milk did not differ with treatments. Reducing the DCAD from -70 to -180 mEq/kg of DM induced a more severe metabolic acidosis, increased ionized Ca concentrations prepartum and on the day of calving, and decreased colostrum yield in the first milking, but had no effects on performance in the subsequent lactation. Collectively, these data suggest that extending the feeding of an acidogenic diet beyond 21 d is unnecessary and might be detrimental to dairy cows, and a reduction in the DCAD from -70 to -180 mEq/kg of DM is not needed.

Use of calcitriol to maintain postpartum blood calcium and improve immune function in dairy cows.

Our objectives were to determine the effects of an injectable formulation of calcitriol on mineral metabolism and immune function in postpartum Holstein cows that received an acidogenic diet prepartum to minimize hypocalcemia. In experiment 1, cows within 6 h of calving received calcitriol (0, 200, or 300 µg) to determine the dose needed to increase plasma concentrations of Ca; 300 µg was sufficient to sustain Ca for at least 3 d. In experiment 2, multiparous cows were assigned randomly to receive only vehicle (control, n = 25) or 300 µg of calcitriol (n = 25) subcutaneously within the first 6 h after calving. Blood was sampled before treatment and 12 h later, then daily until 15 d in milk (DIM), and analyzed for concentrations of ionized Ca (iCa), total Ca (tCa), total Mg (tMg), and total P (tP), metabolites, and hormones. Urine was sampled in the first 7 DIM and analyzed for concentrations of tCa, tMg, and creatinine. Neutrophil function was evaluated in the first week postpartum. Dry matter intake and production performance were evaluated for the first 36 DIM. Calcitriol administration increased concentrations of calcitriol in plasma within 12 h of application from 51 to 427 pg/mL, which returned to baseline within 5 d. Concentrations of iCa and tCa increased 24 h after treatment with calcitriol. Concentrations of iCa (control = 1.08 vs. calcitriol = 1.20 mM), tCa (control = 2.23 vs. calcitriol = 2.33 mM), and tP (control = 1.47 vs. calcitriol = 1.81 mM) remained elevated in cows treated with calcitriol until 3, 5, and 7 DIM, respectively, whereas concentration of tMg (control = 0.76 vs. calcitriol = 0.67 mM) was less in calcitriol cows than control cows until 3 DIM. Concentrations of parathyroid hormone decreased in calcitriol cows compared with control cows (control = 441 vs. calcitriol = 336 pg/mL). Calcitriol tended to increase plasma concentrations of ß-hydroxybutyrate and serotonin, but concentrations of glucose, nonesterified fatty acids, and C-telopeptide of type I collagen in plasma did not differ between treatments. Cows treated with calcitriol excreted more urinary tCa (control = 0.5 vs. calcitriol = 2.1 g/d) and tMg (control = 4.5 vs. calcitriol = 5.0 g/d) in the first 7 and 2 DIM, respectively, than control cows. Compared with control, calcitriol improved the proportion of neutrophils with oxidative burst (control = 31.9 vs. calcitriol = 40.6%), mean fluorescence intensity for oxidative burst (control = 90,900 vs. calcitriol = 99,746), and mean fluorescence intensity for phagocytosis (control = 23,887 vs. calcitriol = 28,080). Dry matter intake, yields of milk, and milk components did not differ between treatments. Administration of 300 µg of calcitriol at calving was safe and effective in increasing blood concentration of iCa and plasma concentrations of calcitriol, tCa, and tP for the first 6 d after treatment, and improved measures of innate immune function in early-lactation Holstein cows.

Quality of life in HIV-positive Brazilians: application and validation of the WHOQOL-HIV, Brazilian version.

The importance of Quality of Life (QOL) evaluation is a recognized outcome in HIV-related studies. The objective of this study was to test the psychometric properties of the Brazilian version of the WHOQOL-HIV. The QOL of 308 HIV-infected men and women was assessed in the different HIV disease severity stages. Women, younger (<35 years) and married patients were associated with a lower QOL. Psychometric properties of the Brazilian version of WHOQOL-HIV were evaluated: reliability, construct validity, discriminant and concurrent validity. Cronbach alpha was above 0.70 in 27 of the 31 facets of the WHOQOL-HIV and ranged between 0.32 and 0.65 in the remaining four facets. Better QOL scores occurred in early stages of the infection (asymptomatic and symptomatic groups) while the AIDS group showed worse scores in all domains of WHOQOL-HIV, with statistically significant differences in early stages. The correlation between the domains and overall QOL was statistically significant (r>0.5; p<0.01). The Brazilian version of the WHOQOL-HIV adequately discriminated between the QOL of individuals in the different stages of HIV infection, in the expected direction and demonstrated satisfactory reliability and concurrent validity in this study. It would appear to be a useful tool to assess the subjective QOL in people living with HIV and AIDS.