Twenty-four newborn Holstein heifer calves were fed 1 of 4 milk replacers (MR): control (20% CP, 21% fat; MR fed at 441 g/d); high protein/low fat (HPLF; 28% CP, 20% fat; MR fed at 951 g/d); high protein/high fat (HPHF; 27% CP, 28% fat; MR fed at 951 g/d); and HPHF MR fed at a higher rate (HPHF+; 27% CP, 28% fat; MR fed at 1,431 g/d). Dry calf starter (20% CP, 1.43% fat) composed of ground corn (44.4%), 48% CP soybean meal (44.4%), cottonseed hulls (11.2%), and molasses (1.0%) was offered free choice. Heifers were obtained from a commercial dairy, blocked by groups of 8 in the order acquired, and randomly assigned to treatments within group. Upon arrival at the research farm, heifers were fed the control for 2 feedings. Treatments were imposed when heifers were 4 +/- 1 d of age. Heifers were on study for 61 +/- 1 d. Body weight and body size measures were taken weekly. Four-day total collection of feed refusals, feces, and urine was initiated at 57 +/- 1 d of age. Heifers were slaughtered at the end of the collection period to evaluate body composition. Preplanned contrasts were used to compare control to all, HPLF to HPHF, and HPHF to HPHF+. Heifers fed the control diet consumed more starter than those fed other treatment diets, but their total dry matter intake and apparent dry matter digestibility were lowest. Fecal output was highest in heifers fed the control diet, whereas urine output and urine N excretion were lowest. Nitrogen intake and urine N excretion were greater for heifers fed HPHF+ compared with HPHF but were not affected by MR fat content (HPLF vs. HPHF). Retention (g/d) of N and P was greater in heifers fed all nutrient-dense diets compared with those fed the control diet, but was not improved by increasing fat in the milk replacer (HPLF vs. HPHF) or by increasing the amount fed. Addition of fat to the milk replacer (HPLF vs. HPHF) increased empty body weight fat content without improving average daily gain or frame measures. Increasing the volume fed (HPHF vs. HPHF+) increased growth rate and empty body weight, but HPHF+ heifers were neither taller nor longer and their carcasses contained more fat. Clear improvements in growth and nutrient retention were observed with more nutrient-dense diets, but most of the improvements were seen with the increased protein intake relative to the control MR; adding fat to the high protein MR did not further improve lean tissue gain.
We investigated the effects of increasing dietary protein and energy on concentrations of selected blood metabolites and hormones in Holstein heifers. Twenty-four heifers were fed 1 of 4 milk replacer (MR) diets for 9 wk (n = 6/diet): control [20% crude protein (CP), 21% fat MR fed at 441 g of dry matter (DM)/d], HPLF (28% CP, 20% fat MR fed at 951 g of DM/d), HPHF (27% CP, 28% fat MR fed at 951 g of DM/d), and HPHF+ (27% CP, 28% fat MR fed at 1,431 g of DM/d). Heifers were fed twice daily; water and starter (20% CP, 1.43% fat) were offered free choice and starter orts recorded daily. Serum and plasma aliquots from blood samples collected twice weekly after a 12-h fast were analyzed for insulin-like growth factor (IGF)-I, IGF-binding proteins (IGFBP), growth hormone (GH), insulin, glucose, nonesterified fatty acids, triglyceride, and plasma urea nitrogen concentrations. Only plasma glucose, IGFBP-2, and IGFBP-3 were affected by diet. Dietary treatment differences were only noted when the control was compared with the average of the other 3 diets. The addition of fat to the MR (HPLF vs. HPHF) and increased volume of MR (HPHF vs. HPHF+) had no effect on plasma glucose concentration or relative abundance of IGFBP-2 or IGFBP-3. Heifers fed the control diet had less glucose, greater IGFBP-2, and less IGFBP-3 than the average of the other 3 diets. There was a diet by week interaction for IGF-I. Serum IGF-I concentration in control heifers varied in a quadratic manner with a nadir (20 +/- 4 ng/mL) at wk 4, whereas IGF-I increased linearly in heifers on other diets. Both insulin and triglyceride changed over time in a complex pattern (significant linear and quadratic contrast effects). The greatest concentrations were measured at wk 0.5 with nadirs at wk 6 for both insulin and triglyceride. Serum GH concentration decreased in a linear manner from wk 0.5 to wk 9 in all heifers. Relative abundance of IGFBP-2 was quadratic over time with the greatest amount of IGFBP-2 observed at wk 5. With the exception of glucose, IGF-I, IGFBP-2, and IGFBP-3, the blood variables measured were not influenced by treatment. The IGF-I -GH-IGFBP axis requires further study in heifers to deduce effects of nutrition on hypothalamic regulation of metabolism. We expected to see more treatment differences in concentrations of metabolites involved with protein and fat metabolism. It is likely that the diets used in this study were not diverse enough in composition to elicit such changes or that the efficiency of use of absorbed protein and fat was not different in these animals.
The objectives of this study were to investigate the effects of the addition of cottonseed hulls (CSH) to the starter and the supplementation of live yeast product (YST) or mannanoligosaccharide product (MOS) to milk, on growth, intake, rumen development, and health parameters in young calves. Holstein (n = 116) and Jersey (n = 46) bull (n = 74) and heifer (n = 88) calves were assigned randomly within sex at birth to treatments. All calves were fed 3.8 L of colostrum daily for the first 2 d. Holstein calves were fed 3.8 L of whole milk, and Jersey calves were fed 2.8 L of whole milk through weaning at 42 d. Calves continued on trial through 63 d. Six treatments were arranged as a 2 x 3 factorial. Calves received either a corn-soybean meal-based starter (21% crude protein and 6% acid detergent fiber; -CSH) or a blend of 85% corn-soybean meal-based starter and 15% CSH (18% crude protein and 14% acid detergent fiber; +CSH) ad libitum. In addition, calves received whole milk with either no supplement (NONE) or supplemented with 3 g/d of mannanoligosaccharide product (MOS) or 4 g/d of live yeast product (YST) through weaning at 42 d. Twelve Holstein steers [n = 6 (per starter type); n = 4 (per supplement type)] were euthanized for collection and examination of rumen tissue samples. Dry matter intake (DMI) was greater for Holstein calves fed +CSH (0.90 kg/d) than -CSH (0.76 kg/d). Final body weight at 63 d of Holstein calves fed +CSH (75.8 kg) was greater than that of those fed -CSH (71.0 kg). Average daily gain (ADG) was greater for Holstein calves fed +CSH (0.58 kg/d) than -CSH (0.52 kg/d). However, Holstein calves fed -CSH had a greater feed efficiency (FE; 0.71 kg of ADG/kg of DMI) than those fed +CSH (0.65 kg of ADG/kg of DMI). Also, Holstein calves fed +CSH had narrower rumen papillae (0.32 mm) compared with those fed -CSH (0.41 mm). There were no significant effects of CSH on DMI, ADG, or FE in Jersey calves. There were no significant effects of YST or MOS on DMI, ADG, FE, or rumen papillae measures in Holstein calves. Jersey calves fed YST or MOS had greater final body weight at 63 d (51.2 kg and 51.0 kg, respectively) than calves fed NONE (47.5 kg). However, there were no significant effects of YST or MOS on DMI, ADG, or FE in Jersey calves.
A dynamic, mechanistic, compartmental model of phosphorus (P) digestion and metabolism was constructed in the Advanced Continuous Simulation Language using conservation of mass principles and mass action kinetics. Phosphorus was assumed to exist in 3 forms: inorganic (Pi), phytic acid (Pp), and organic (excluding phytic acid; Po). All 3 forms were assumed to be present in the digestive tract with absorption of Pi into blood. Inputs to the model were total P intake; Pp, Po, and Pi as proportions of total P; milk yield; rate of salivation (fixed at 239 L/d); and rate of liquid passage from the rumen (fixed at 198 L/d). The model was fitted to 2 experiments from the literature. Derived parameters were well defined by the data. With a mean observed P intake of 75 g/d, total tract P digestibility was 38%. Phytic acid P digestibility in the rumen was 74%, with no additional Pp digestion in the lower tract. Inorganic P and Po digestibility in the lower tract were 48 and 89%, respectively. Flows of Po and Pi from the rumen were 2.4 and 3.0 times greater than intake, respectively. The increase in Po was apparently due to microbial growth. The increase in Pi arose primarily from secretion of Pi into the rumen via salivation where 65% of absorbed P was recycled to the rumen. Milk synthesis used 30% of absorbed Pi, and 1% was excreted in urine. This research suggested that the primary regulation points for maintaining blood P were bone deposition and resorption and absorption from the intestine. However, because bone P balance was related to both dietary P intake and ruminal phytase activity, it is critical to achieve a better understanding of phytate digestibility across several feeds if dietary P is to be reduced below current requirements.
Human antigen R (HuR) is a nucleocytoplasmic shuttling protein that binds to and stabilizes mRNAs containing adenine- and uridine-rich elements. Under normal growth conditions, the bulk of HuR is maintained in the nucleus, but under conditions of cell stress, HuR may become more prevalent in the cytosol, where it can stabilize mRNA and regulate gene expression. We have studied the behavior of HuR in LLC-PK1 proximal tubule cells subjected to ATP depletion and recovery. ATP depletion resulted in detectable net movement of HuR out of the nucleus, followed by net movement of HuR back into the nucleus on reversion to normal growth medium. In addition, HuR protein levels increased during energy depletion. This increase was inhibited by cycloheximide and was independent of HuR mRNA levels, since no change was noted in the quantity of HuR transcript. In contrast, recovery in normal growth medium resulted in increased HuR mRNA, while protein levels decreased to baseline. This suggested a mechanism by which previously injured cells maintained normal levels of HuR but were primed to rapidly translate increased amounts of protein on subsequent insults. Indeed, a second round of ATP depletion resulted in heightened HuR protein translation at a rate more rapid than during the first insult. Additionally, the second insult produced increased HuR levels in the cytoplasm while still maintaining high amounts in the nucleus, indicating that nuclear export may not be required on subsequent insults. These results suggest a role for HuR in protecting kidney epithelia from injury during ischemic stress.
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