| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Dairy Science, Virginia Polytechnic Institute and State University, Blacksburg 24061
1 Corresponding author: rma{at}vt.edu
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
Key Words: blood metabolite • dairy calf • milk replacer
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
A major focus is the impact of energy and protein intake on the growth hormone (GH)-IGF-1 axis as others have emphasized (Breier et al., 1988; Hammon and Blum, 1997; Smith et al., 2002). This is because of well-recognized effects of these molecules on nutritional physiology, body growth, and mammary development. Growth hormone concentration is typically reduced and IGF-I elevated in well-fed heifers. However, the activity of IGF-I is regulated by IGF binding proteins (IGFBP). Irrespective of diet, both IGF-I and GH are temporally regulated in heifers, with circulating GH concentration greater in neonates but reduced in postnatal life. We sought to measure circulating GH, IGF-I, and IGFBP in heifers fed different diets to evaluate these temporal and nutritional relationships and additionally associate changes with calf performance and measures of growth and body composition reported in Hill et al. (2008).
Blood metabolites are traditional and accepted indicators of nutritive status and metabolism. Diaz et al. (2001) suggested that altering the carbohydrate and fat content of MR might increase the biological value of absorbed protein. We hypothesized that regulators of carbohydrate, protein, and lipid metabolism such as the GH–IGF-I axis molecules would be affected by our dietary treatments and that these alterations would be mirrored by changes in concentrations of circulating hormones and metabolites. We also anticipated that changes in these hormones and metabolites would correspond with heifer performance. We chose to measure serum total protein and plasma urea nitrogen (PUN) to evaluate protein metabolism and NEFA and triglyceride concentrations as indices for fat metabolism.
In preweaned heifers, glucose and insulin concentrations are typical of mammalian monogastrics, whereas concentrations of VFA are proportionally reduced but increase with time and starter intake. In older ruminants both glucose and insulin concentrations are reduced whereas VFA concentrations are proportionally increased. Quigley et al. (1991) demonstrated that plasma glucose declined with age and also with early weaning. We expected that differences would be evident in glucose and insulin concentrations in heifers fed various MR formulations coupled with ad libitum starter intake and that these differences would be associated with DMI.
The objectives of this experiment were to investigate effects of altering dietary protein and energy on concentrations of selected blood metabolites and hormones in Holstein heifers between 1 and 9 wk of age. A secondary objective was to examine the relationship between concentrations of metabolites and hormones with overall calf performance.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
Upon arrival at the Virginia Tech Dairy Center, subcutaneous injections of 4 mL of Excenel (Pharmacia and Upjohn Company, Kalamazoo, MI), 3 mL of BoSe (1 mg of selenium and 68 IU/mL of vitamin E, Schering-Plough Animal Health Corp., Union, NJ), 1 mL of vitamins A and D (500,000 IU/mL of vitamin A; 75,000 IU/ mL of vitamin D, Vedco Inc., St. Joseph, MO) were administered. Additionally, all animals received an intranasal dose of 2 mL of TSV-2 (Pfizer Animal Health, New York, NY); at 9 d all animals received an intramuscular injection of 2 mL of Pyramid 4 (Fort Dodge Animal Health, Overland Park, KS).
Heifers were individually housed in open hutches bedded with loose gravel for wk 1 through 8. At wk 9 they were moved to individual metabolism stalls for total collection of feces and urine (Hill et al., 2008). One heifer (group 1; on high-protein, low-fat MR) died unexpectedly at 6 wk of age from acute peritonitis and endotoxemia that resulted from a perforated abomasal ulcer; that animal was not replaced and data from her were excluded. All animals were sacrificed at approximately 64 d of age to evaluate mammary development and body composition (K. M. Daniels, unpublished data; Hill et al., 2008). At the time of slaughter, it was noted that a heifer (group 3; on control MR) had an irregularly shaped reproductive tract and underdeveloped mammary tissue. This heifer was suspected to be a freemartin; her hormone and metabolite data were retained. Additionally, just before harvest, 2 other calves (group 1; on high-protein, high-fat MR fed at the higher rate) showed symptoms of urinary tract infection, were treated with intravenous fluids and antibiotics, and survived until harvest.
Diets and Feeding.
Dietary MR treatments were randomly assigned within each group. The MR treatments used in this trial were control (CON; 20% CP, 21% fat MR fed at 441 g of DM/d), high-protein/low-fat MR (HPLF; 28% CP, 20% fat MR fed at 951 g of DM/ d), high-protein/high-fat MR (HPHF; 27% CP, 28% fat MR fed at 951 g of DM/d), and HPHF MR fed at a higher rate (HPHF+; 27% CP, 28% fat MR fed at 1,431 g of DM/ d). Analyzed values of MR and average daily intakes are reported in Table 1
. All MR powders used in the experiment were obtained from Land O’Lakes Inc. Animal Milk Products Co., were nonmedicated, and contained whey protein as the protein source. Animal tallow was the fat source used in all MR. Animals were fed MR treatment diets reconstituted to 12.5% solids at 0700 and 1900 h from nipple buckets. Total volume of the HPHF MR was increased 1.5 fold to increase intake in heifers fed HPHF+. Heifers were offered fresh water and starter free choice. Calf starter (20% CP, 1.43% fat) comprised ground corn (44.4%), 48% CP soybean meal (44.4%), cottonseed hulls (11.2%), and molasses (1.0%). Starter orts were recorded daily at the evening feeding. Milk replacer refusals, if any, were recorded at each feeding. Dietary MR treatments commenced at the morning feeding the day after arrival; if heifers were less than 1 d old they received one additional feeding of a 20% CP, 21% fat MR before switching to their assigned treatment diet. All heifers received 30 g/d of Gammulin powder (APC Inc.) in the morning milk replacer through 10 d of age.
|
Blood Collection and Analysis
Initial IgG Determination.
A single jugular blood sample was drawn from each animal upon arrival to determine IgG concentrations in serum as an indicator of passive immunity. Single radial immunodiffusion kits (VMRD Inc., Pullman, WA) were used to measure IgG. Samples were run in duplicate in a single assay; the intraassay CV was 12%.
Blood Collection and Processing.
Blood was collected from each animal on Wednesdays and Saturdays before the morning feeding (after a 12-h fast). Jugular blood samples (
25 mL total) were collected into evacuated tubes containing sodium heparin and sodium fluoride, and a tube with no anticoagulant. All samples were kept on ice after collection and were transported to the laboratory within 1 h. Immediately after arrival at the laboratory, aliquots of sodium-heparinized blood (30 µL) were used for determination of packed cell volume (PCV) via the microhematocrit method. The remaining portion of the sodium heparin samples and the sodium fluoride samples were centrifuged at 2,000 x g at 4°C for 20 min. After centrifugation, plasma was decanted into individually labeled 12- x 75-mm polypropylene tubes, and stored in a –20°C freezer for future analyses of PUN (sodium heparin samples) and glucose (sodium fluoride samples). Tubes without anticoagulant were allowed to clot at room temperature for 3 to 6 h, after which time they were placed in a 4°C refrigerator for 24 h. Tubes were then centrifuged at 2,000 x g at 4°C for 20 min; serum was decanted into individually labeled 12- x 75-mm polypropylene tubes, and stored at –20°C for future analyses of IGF-I, GH, insulin, IGFBP, total protein, NEFA, and triglycerides (TRI).
Hormone and IGFBP Analyses.
Serum IGF-I, GH, and insulin concentrations were determined in all samples via double-antibody RIA. For the IGF-I assay, acid-ethanol extraction of binding proteins (Sharma et al., 1994) preceded RIA. Insulin and GH assays were conducted as in McFadden et al. (1990); the IGF-I assay was performed according to Weber et al. (1999) and Berry et al. (2003). Briefly, for the IGF-I assay recombinant human IGF-I (GrowPrep, Adelaide, Australia) was used for iodination and standards. Mouse anti-human IGF-I primary antibody was a gift from Bernard Laarveld (University of Saskatchewan, Saskatchewan, Canada) and was used at a final dilution of 1:70,000. Commercial goat anti-mouse secondary antibody (Sigma Chemical Company, St. Louis, MO) was used at a final dilution of 1:20. For the GH assay, recombinant bovine GH (lot 6958C-42A, American Cyanamid Company, Princeton, NJ) was used for standards and iodination. Rabbit anti-ovine GH (NIDDK-anti-oGH-2; AFP-C0123080; gift from the National Hormone and Pituitary Program, Baltimore, MD) was used as the primary antibody at a final dilution of 1:100,000. Ovine anti-rabbit gamma globulin antiserum was used at a final dilution of 1:15. For the insulin assay, purified bovine insulin (lot 615-70N-80; Eli Lilly and Co., Indianapolis, IN) was used for iodination and standards. Guinea pig anti-bovine insulin (lot GP20) was the primary antibody (Miles Laboratory, Elkhart, IN) and used at a final dilution of 1:12,000. Ovine anti-guinea pig gamma globulin antiserum was used at a final dilution of 1:20. Intra- and interassay CV were less than 8 and 8% for the IGF-I RIA, 8 and 10% for the GH RIA, and 9 and 9% for the insulin RIA.
Western ligand blotting of wk 1, 5, and 9 (Saturday) serum samples was used to determine relative abundance of IGFBP and was performed essentially according to Berry et al. (2003). Briefly, a molecular weight marker (Precision Plus Protein Standards, Bio-Rad Laboratories, Hercules, CA), 16 µg of purified IGFBP-3, 4 µL of a calf serum pool, and 6 serum samples (6 µL per lane in duplicate) were run in 15 lanes on a vertical slab gel unit (Hoefer Scientific Instruments, San Francisco, CA). Two gels were electrophoresed at the same time. Samples were dissolved into nonreducing SDS-PAGE buffer and electrophoresed through 12% SDS-PAGE gel at 65 V for 18 h. After electrophoresis, proteins were electrotransferred (55 V, 5 h) to nitrocellulose membranes and incubated in 125I-IGF-I (1 x 106 cpm/mL) overnight and washed in Tris-buffered saline to remove unbound ligand. Blots were exposed to Kodak x-ray film for 24 h at –80°C. Scanning densitometry was used to quantify changes in IGFBP profiles. Purified IGFBP-3 and an aliquot of a serum pool served as positive controls on each gel.
Biochemical Analyses.
Serum total protein quantification was based on the Biuret color reaction (Total Protein Biuret Reagent Set, Pointe Scientific Inc., Canton, MI) and was scaled for use in a 96-well microtiter plate. An aqueous protein standard (8 g/dL, Pointe Scientific Inc.) was used in the assay. Intra- and interassay CV for serum total protein were less than 3 and 3%, respectively. Serum TRI were determined using an enzymatic assay kit (Triglycerides-GPO Reagent Set, Pointe Scientific Inc.) with volumes scaled for use in a 96-well microtiter plate. An aqueous triglyceride standard (200 mg/dL, Pointe Scientific Inc.) was used in the assay. Intra- and interassay CV for serum TRI were less than 5 and 8% respectively. Plasma glucose was analyzed by enzymatic determination (Autokit Glucose, Wako Diagnostics, Richmond, VA) using the Wako Glucose C2 Microtiter procedure. Intra- and interassay CV for plasma glucose were less than 4 and 3%, respectively. Plasma urea nitrogen was determined according to the method of Chaney and Marbach (1962) as modified by Weatherburn (1967), except that urease concentration was 10-fold greater than recommended. Intra-and interassay CV for PUN were less than 4 and 4%, respectively. Plasma NEFA were analyzed by enzymatic determination using NEFA C kits purchased from Wako Chemicals and the Wako NEFA C Microtiter procedure. Intra- and interassay CV for plasma NEFA were less than 2 and 2%, respectively.
Statistical Analyses
Initial IgG concentration data were analyzed using the Mixed procedure of SAS (SAS Version 9.1.3, SAS Institute, Cary, NC); diet, group, and their interaction were the fixed effects and heifer within diet and group was the random term.
Hormone and metabolite data were analyzed using the Mixed procedure of SAS with repeated measures. The repeated measure was week and the subject used in tests was heifer within diet and group. An autoregressive covariance structure [AR(1)] was used throughout analyses; no denominator degrees of freedom approximation method was specified. Twice-weekly hormone and metabolite data were averaged within week before analyses in all weeks except wk 0. Zero-week samples were not averaged because animals were not on their treatment diets for half of the week; wk 0 then represents data from a single blood draw obtained within 2 d of treatment initiation, and is referred to as wk 0.5. Data are reported as least squares means ± standard errors. The interaction of group and week and the 3-way interaction of diet by group by week were considered, but were removed from the final model due to lack of significance. Preplanned nonorthogonal contrast statements were used to examine diet differences when present; they were CON vs. all other treatments; HPLF vs. HPHF; and HPHF vs. HPHF+. Group means were separated with a Tukey test. Orthogonal polynomial contrasts were used to test for linear and quadratic responses over time. The correlation procedure of SAS was used to determine relationships of selected variables. Significance was declared at P < 0.05 for all procedures. The following model statement was used for all analyses:
 |
where Yijkl = dependent variable; µ = overall mean; Di = fixed effect of diet (i = 1,..,4); Gj = fixed effect of group (j = 1, 2, 3); Wk = fixed effect of week (k = 1,...,10) (IGFBP, k = 1, 2, 3); H(ij)l = random effect of heifer within diet and group; (DG)ij = fixed interaction of diet and group; (DW)il = fixed interaction of diet and week; and e(ijk)l = residual error (assumed to be random and independently distributed).
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
). These consisted of 3 heifers in group 2 (CON, HPLF, and HPHF+) and 2 heifers in group 3 (CON and HPHF).
|
). Heifers on the HPLF, HPHF, and HPHF+ diets did not differ in their IGF-I response to diet.
|
and Table 3, respectively). Overall, heifers fed CON had lower glucose, greater IGFBP-2, and lower IGFBP-3 than the average of the other 3 diets (Figure 2).
|
|
). Correspondingly, all heifers showed a linear decrease in fecal score over time (2.0 ± 0.13 at wk 0.5 and 1.1 ± 0.21 at wk 9; P < 0.001; Table 4). Both insulin and TRI changed over time in a complex pattern (significant linear and quadratic contrast effects). The greatest insulin and TRI concentrations were recorded at wk 0.5 and apparent nadirs were observed at wk 6 for both variables (Table 5). Serum GH concentration decreased in a linear manner from wk 0.5 to wk 9 (Table 5; 8.9 to 4.4 ± 1.16 ng/mL; P < 0.001) in all heifers. Relative abundance of IGFBP-2 was affected by week (P = 0.053) and was quadratic over time (P = 0.023) with the greatest amount of IGFBP-2 observed at wk 5 (Table 3
).
|
|
). Serum protein concentrations for heifers that arrived on August 20 (group 1) were not different from the other 2 groups (Table 5).
Correlations
Overall, PCV was not correlated with fecal score (r = 0.13; P = 0.084). Serum IGF-I concentration was positively correlated with relative abundance of IGFBP-3 (r = 0.40; P = 0.012), negatively correlated with relative abundance of IGFBP-2 (r = –0.21; P = 0.001), and unrelated to IGFBP-5 and IGFBP-4. Serum GH was not correlated with relative abundance of any IGFBP. Serum GH was negatively correlated with serum IGF-I (r = –0.24; P = 0.01).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
). Additionally, although the main effect of diet cannot be separated for serum IGF-I because there was a significant diet by week interaction, it is evident that heifers on CON displayed a different pattern of IGF-I concentration over time compared with heifers reared on the other 3 diets (Figure 1).
We attribute the diet difference in plasma glucose to increased starter intake in CON. Starter is known to promote rumen development and hence hasten the transition from an essentially monogastric animal (high blood glucose) to a functional ruminant (low blood glucose). However, glucose concentration only tended to be affected by time in our study (P = 0.077). We speculate that because CON animals already had lower plasma glucose concentrations than animals on the other 3 dietary treatments at wk 0.5 (likely a reflection of the lower MR intake), this proportional difference was maintained throughout the study, thereby nullifying a treatment by week interaction. Also, our animals were still being fed MR at 9 wk of age; this likely increased plasma glucose and prevented a decline to concentrations typical of fully weaned ruminant animals. Insulin and glucose are intimately linked; however, we did not detect a diet effect on insulin (Table 5). We suspect that our sampling protocol prevented us from being able to detect divergent insulin concentrations in these heifers. Insulin values reported here were obtained after the animals were subjected to a 12-h fast, were low, and approached the sensitivity limits of the assay. In calves, circulating insulin concentration typically peaks 2 to 4 h postfeeding; our data in contrast reflect baseline insulin rather than a meal response. Smith et al. (2002) presented plasma insulin concentrations for Holstein bull calves fed a 30% CP, 20% MR to achieve target rates of gain of 0.50, 0.95, or 1.40 kg/d (low, medium, and high, respectively). They collected blood samples 4 to 6 h after the morning feeding (from Diaz et al., 2001) and noted that plasma insulin concentrations were distinctly increased with augmented nutrient intake and appeared to sufficiently control circulating glucose (Smith et al., 2002). Had we chosen to sample blood 4 to 6 h postfeeding, perhaps we would have noted diet differences.
Insulin-like growth factor binding proteins modulate the effects of IGF-I. The IGFBP detected in serum included bands at approximately 44, 40, 34, 31, 29, 28, and 24 kDa. Although specific antibodies and deglycosylation techniques were not used to identify individual IGFBP bands, it can be deduced from previous studies that the 44- and 40-kDa bands were 2 different glycosylated forms of IGFBP-3, the 34 kDa band was IGFBP-2, IGFBP-5 migrated as a doublet at approximately 29 to 31 kDa, and the 24- and 28-kDa bands were nonglycosylated and glycosylated forms of IGFBP-4, respectively (Cohick et al., 1996; Funston et al., 1996; Roberts et al., 1997). The 44- and 40- kDa bands of IGFBP-3 and the 31- to 29-kDa bands of IGFBP-5 were not always distinguishable as individual bands on ligand blots. Therefore, IGFBP activity in those regions of ligand blots was analyzed as singular bands. Relative abundance data submitted for statistical analysis included values for IGFBP-3, IGFBP-2, IGFBP-5, and IGFBP-4 (28 kDa and 24 kDa analyzed separately). Here, we measured an effect of diet on relative abundance of IGFBP-2 and IGFBP-3, but not IGFBP-4 or IGFBP-5. Heifers on CON had relatively more IGFBP-2 and less IGFBP-3 than the average of the other 3 diets (Table 3).
Dietary treatments of MR, MR + recombinant human IGF-I, or colostrum for 2 d followed by MR had no effect on IGFBP profiles in the first week of life in neonatal calves (Skaar et al., 1994). Those authors attributed the lack of effect to being a reflection of the minimal effects of dietary IGF-I on circulating IGF-I concentrations in the early days of life (Baumrucker and Blum, 1994) and perhaps low animal numbers in the experiment (n = 16). Consistent with the findings of Skaar et al. (1994), we found IGFBP-3 to be the predominant IGFBP in circulation at all times measured and across all dietary treatment groups. In addition to evaluating diet effects on IGFBP profiles in neonatal calves, Skaar et al. (1994) analyzed the ontogeny of IGFBP from birth to 45 wk of age, because changes in IGFBP were observed within the first week of life in all calves regardless of diet. Ligand blot analysis was conducted on plasma from calves that were 1, 12, 24, and 45 wk old (infant, juvenile, pre-, and postpubertal, respectively; Skaar et al., 1994). They found that expression of IGFBP-2 peaked at 12 wk with a decrease to 45 wk to a concentration similar to that at wk 1. The relative abundance of IGFBP-3 continually increased from 1 to 45 wk of age as did IGF-I concentrations (Skaar et al., 1994). In our 9-wk study, relative abundance of IGFBP-3 did not change over time (assessed at 3 time points), but IGFBP-2 did (Table 3). Relative abundance of IGFBP-2 was quadratic over time (P = 0.023) with the greatest amount of IGFBP-2 observed at wk 5 (Table 3). This quadratic trend is consistent with Skaar et al. (1994), who reported a quadratic response of IGFBP-2 concentration over time, although their apparent nadir was observed at wk 12 of life. The exact physiological role of IGFBP-2 is still unclear, but postnatal decreases in concentrations of IGFBP-2 have been noted in other species (Donovan et al., 1989; Owens et al., 1991) and are likely related to IGF-I availability and action during growth and development (Skaar et al., 1994).
In addition to being a positive regulator of body growth, IGF-I has been shown to affect circulating IGFBP profiles (Clemmons et al., 1989; Zapf et al., 1989, 1990). Here, we observed CON to have reduced IGF-I concentration over time compared with the average of the other 3 diets, with a corresponding increase in IGFBP-2 and decrease in IGFBP-3. We found serum IGF-I to be positively correlated with serum IGFBP-3, negatively correlated with IGFBP-2, and unrelated to IGFBP-4 and IGFBP-5.
Endogenous GH is a major regulator of circulating IGF-I. In calves, as in many species, GH concentration decreases during the first year of life at a time when IGF-I and IGFBP-3 both increase. This indicates that factors other than GH control IGF-I and IGFBP-3 concentrations. Concentration of circulating GH was not affected by diet in our calves despite clear dietary effects on IGF-I, IGFBP-3, and IGFBP-2. Circulating GH is known to be secreted in a pulsatile manner throughout the day. Our sampling protocol did not employ multiple blood draws throughout the day to account for this, but values obtained were within the physiologically normal preprandial range for young dairy animals (Hammon et al., 2002; Nussbaum et al., 2002; Quigley et al., 2006). Regardless, our GH data do not suggest an effect of diet (Table 5). We measured a decline in serum GH over time, which is consistent with results of others (Hammon and Blum, 1997; Hammon et al., 2002; Quigley et al., 2006) and is attributed to normal physiological events. In cattle, as with most species, feed restriction usually causes an increase in circulating GH. Had we restricted the starter intake in CON we would have likely seen an increase in GH concentration in those animals.
Although perhaps not an ideal model for the heifer calf but worth mention, the model of Vicini et al. (1991) showed that dietary restriction or periods of negative energy balance are associated with increased circulating IGFBP-2 and decreased IGFBP-3 in ruminants. Similarly, in a study designed to evaluate nutritional influences on reproductive function in beef cattle, Roberts et al. (1997) noted that cows that failed to resume cycling postpartum had lower circulating IGF-I, greater amounts of IGFBP-2, and lesser amounts of IGFBP-3 at wk 2 postpartum compared with cows that resumed cycling during that time. Nutritional suppression of the GH–IGF-I axis in CON is probable and therefore this axis likely alters circulating IGFBP-2 and IGFBP-3. The physiological significance of IGFBP in serum, especially as it relates to animals reared on CON, remains to be determined. One proposition is that changes in the GH–IGF-I–IGFBP axis occur in response to nutritional stress and that these changes provide a signal to the hypothalamus to perceive changes in metabolic status (Roberts et al., 1997). It remains to be determined what divergent roles, if any, IGFBP-2 and IGFBP-3 played in CON compared with the other 3 dietary treatments.
The diets used in this experiment were designed to differ in energy and protein content; therefore, we thought that markers for protein and fat metabolism (PUN, NEFA, TRI) would be affected by diet, but they were not (Table 5). Feeding a diet that supplies more protein than the animal can utilize should result in elevated PUN. Here, PUN was not affected by diet or by any other model effect tested. Terosky et al. (1997), Smith et al. (2002), and Bartlett et al. (2006) also noted no change in PUN over time or with respect to imposed dietary treatments, and reported PUN concentrations similar to ours. More N was supplied to heifers fed HPHF+ than to those fed HPHF, which was the goal of the treatment design. A companion paper (Hill et al., 2008) showed that heifers fed the HPHF+ diet consumed 15.2 g/d more N than those fed HPHF, but N retention was unchanged because most of the excess N was excreted in urine. This agrees with PUN data and suggests that liberal intake of a high-protein, high-fat MR is not recommended for practical purposes and results in excess nutrients being lost to the environment. Bascom et al. (2007), Tikofsky et al. (2001), and Bartlett et al. (2006) have all reported elevated NEFA in bull calves fed high-fat MR compared with cohorts fed MR with lower fat, and this is attributed to the fat source of the high-fat MR (edible lard as opposed to milk fat). The fat source was the same for all MR used in this experiment (edible lard), which might explain why no differences in NEFA were detected (Table 5). Additionally, elevated NEFA are a hallmark sign of adipose tissue catabolism. Because NEFA were unaffected by diet, this suggests that feed intake in all dietary treatment groups provided sufficient energy supply preceding the next MR meal, even in CON. Last, because the MR feeding frequency was the same for all dietary treatments in this experiment, the lack of diet effects on plasma TRI (Table 5) implies little, if any, difference among treatments on frequency of starter consumption by our heifers. Pancreatic lipase activity and efficiency of TRI clearance also affect plasma TRI concentrations. Plasma TRI was similar and deposition of body fat greater (Hill et al., 2008) when heifers were fed HPHF+ compared with HPHF. These observations indicate that pancreatic lipase activity was sufficient to facilitate absorption of a substantial amount of the additional dietary fat and this addition of dietary fat did not overwhelm TRI clearance.
A secondary objective of this experiment was to examine the relationship between concentrations of metabolites and hormones with overall calf performance. We chose to use PCV and fecal scores for this purpose. Packed cell volumes reported here are similar to those reported elsewhere for calves of this age (Terosky et al., 1997; Lesmeister et al., 2004; Lesmeister and Heinrichs, 2005). All heifers showed a linear increase in PCV and a linear decrease in fecal score over time (Table 4). Overall, PCV was not correlated with fecal score (r = 0.13; P = 0.084). We speculated that PCV and fecal score would be positively correlated, considering that heifers with watery feces (fecal scores of 3 to 4) are more likely to be dehydrated and therefore have greater PCV. The electrolyte therapy used in this study may have prevented dehydration in scouring heifers, thereby keeping PCV within the physiologically normal range for preweaned heifers.
Failure of passive transfer, assessed at approximately 2 d of age, was detected in 5 calves (22%) despite implementation of a colostrum management protocol (Table 2). Calves with failure of passive transfer were dispersed between group 2 (CON, HPLF, and HPHF+) and group 3 (CON and HPHF), with no difference in IgG concentration detected between the 3 purchase groups. Because calves with failure of passive transfer were present in all dietary treatment groups, our results are not biased by IgG status. Serum protein differed by purchase group in our animals (Table 5); however, when wk 0.5 samples were analyzed separately with IgG data, serum protein was not affected by diet, group, or their interaction (data not shown). Moreover, wk 0.5 serum protein values were positively correlated with IgG concentration (r = 0.528; P = 0.012). Serum protein concentration did not change over time or with diet in these heifers, but was still affected by purchase group (Table 5). The third group of heifers had fewer general health ailments (data not shown) than the other 2 groups and it is speculated that the increased serum total protein concentration reflects this result. Because most of the protein found in serum is albumin, we can infer that hepatic synthesis of albumin was not affected by diet in this experiment, but appears to have been affected by calf health. Similar to our findings, Terosky et al. (1997) noted no change in serum protein over time or with dietary treatment in similarly aged bull calves. Conversely, Bartlett et al. (2006) noted differences in concentration of total protein in plasma for calves fed varying amounts of dietary CP (14 to 26%) in MR at 1 of 2 intake levels (1.25 or 1.75% of BW) and attributed these differences to protein malnutrition in the animals with lower plasma protein concentrations. Because we detected no differences in serum protein with diet, we can infer that protein malnutrition was not experienced in this experiment.
|
CONCLUSIONS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
|
ACKNOWLEDGEMENTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
Received for publication November 13, 2007. Accepted for publication February 29, 2008.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. R. Hill, K. F. Knowlton, K. M. Daniels, R. E. James, R. E. Pearson, A. V. Capuco, and R. M. Akers Effects of Milk Replacer Composition on Growth, Body Composition, and Nutrient Excretion in Preweaned Holstein Heifers J Dairy Sci, August 1, 2008; 91(8): 3145 - 3155. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
