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One hundred forty spring-born Angus × Gelbvieh and purebred Angus steers were selected for study as early weaned (EW; average age at weaning = 90 ± 30 d) or traditionally: weaned (TW; average age at weaning = 174 ± 37 d) steers that were nonimplanted or implanted (Synovex-S, Fort Dodge Animal Health, Overland Park, KS). Initially, steers were sorted by age, sire, and farm, and then allotted randomly in a 2 × 2 factorial arrangement of treatments of EW implanted (EWI), EW nonimplanted (EWN), TW implanted (TWI), or TW nonimplanted (TWN). Ultrasound measurements (US) of LM area (LMA), 12th rib fat thickness (US-BF), and marbling (US-M) were collected every 28 d during the time that steers were on feed. At 202 d of age, EW calves had larger US-LMA, US-BF, and BW than TW calves (37.9 vs. 32.3 cm², 0.38 vs. 0.26 cm, and 271.6 vs. 218.9 kg, respectively; P < 0.001). At slaughter, EW calves had heavier HCW (290.4 vs. 279.7 kg, respectively; P < 0.05) and greater USDA marbling scores (51.25 vs. 46.26, respectively; P < 0.05) than TW calves; more EW steers graded USDA Choice or greater (P = 0.05). However, no differences were detected in BW (P = 0.15), LMA (P = 0.39), BF (P = 0.45), or liver abscess scores (P = 0.41). Twenty-four implanted steers were selected from the original group of 140 and sorted into two slaughter groups of 12. Twelve implanted steers from each weaning group, matched in slaughter BW but differing in age, were subsampled at slaughter to assess the effect of weaning age and chronological age on muscle tenderness. Younger animals had lower Warner-Bratzler shear force values (P < 0.001) than older calves after 14 d of postmortem aging; however, no differences were found in tenderness after 21 d of aging. Furthermore, there was greater variance (P < 0.001) in Warner-Bratzler shear force values among younger, EW steers vs. older, TW steers. These data provide evidence that early weaning of beef calves may be used as a tool to more effectively manage the cow-calf production system without compromising the quality of the offspring. [ABSTRACT FROM AUTHOR]

A deficit in bone development during early life has been associated with increased likelihood of developing osteoporosis later in life. Dietary Ca and phosphate play a pivotal role in bone development, which is largely orchestrated by the cellular activities osteogenesis, ostoclastogenesis, and adipogenesis. This study aims to determine the impact of different concentrations of dietary Ca and phosphate supplementation on bone development and mesenchymal stem cell (MSC) programming. Twenty-seven newborn neonatal pigs (n = 27; 24 ± 6 h) were randomly assigned into 3 groups and received a milk replacer diet for 16 d. Diets were isonitrogenous and isocaloric but had varying concentrations of Ca and phosphate. The diets were designed to be 25% deficient, adequate, or 25% in excess (NRC standard) of Ca and phosphate requirements. Bone mineral content, serum mineral and hormone concentrations, and activity of MSC were determined. Serum phosphate concentrations were significantly higher in pigs receiving the adequate diet compared with those fed the deficient diet on d 8 but lower among pigs fed the excess diet compared with those fed the deficient diet on d 16 (P < 0.05). Serum FGF23 concentrations were greater among the pigs fed the deficient diet than those fed the excess diet on d 16 (77.21 ± 1.90 vs. 70.38 ± 1.90 pg/mL; P < 0.05). Pigs receiving the diet containing excess Ca and phosphate had significantly higher bone ash and bone volume compared with the deficient group. We determined in vivo proliferation of the MSC with BrdU, and there was greater cell proliferation in pigs fed the adequate diet than in those fed the deficient diet (8.9% ± 0.7 vs. 6.3% ± 0.7; P < 0.05). Calcium and phosphate deficiency shifted MSC towards adipogenic differentiation, as indicated by both Oil Red O staining and increased gene expression of key adipogenic factors such as PPARγ2, FABP4, and LPL. Meanwhile, osteogenesis in the deficient group was reduced compared with adequate group, which was illustrated by lower expression of master osteogenic regulator osteocalcin. This study demonstrates the importance of even minor deficiencies in neonatal Ca and phosphate intake and their impact on bone mineral acquisition and in shaping MSC activity and lineage allocation. [ABSTRACT FROM AUTHOR]

Postnatal skeletal muscle growth requires satellite cell activation and fusion with existing myofibers. Delay or absence of satellite cell proliferation and differentiation leads to a reduction in postnatal muscle hypertrophy and reduced growth potential. Calcium and phosphate are necessary for normal muscle development, and deficiencies cause altered satellite cell function and reduced muscle accumulation. Dietary PO4 deficiencies were shown to cause decreased satellite cell proliferation in vitro whereas excess PO4 caused increased proliferation. The objective of this study was to determine proliferation and differentiation of satellite cells in response to combined Ca-PO4 deficient, adequate, and excess diets in neonatal pigs. Twenty-seven newborn piglets (24 ± 6 h age) were assigned to dietary treatments, based on NRC requirements, containing an adequate Ca-PO4 available diet, a 25% deficient Ca-PO4 available diet, or a 25% excess Ca-PO4 available diet over a 17-d trial. Feed intake and BW were recorded daily, and blood samples were collected at 8 and 16 d. Oral bromodeoxyuridine (BRDU) was administered 18 h prior to sacrifice. Following sacrifice, longissimus dorsi muscle was collected for immunohistochemistry and satellite cell (SC) isolation. Isolated SC were cultured for in vitro proliferation and differentiation assays. Dietary treatments altered serum phosphate whereas adequate treatment increased serum phosphate by 8% compared with the deficient diet at 8 d but was 12% less in the excess diet compared with the deficient at 16 d (P < 0.05). There were no differences in ADG between treatments (P = 0.16). Dietary deficiency reduced proliferating satellite cells (BRDU/MyoD+) in vivo (P = 0.02) compared with adequate and excess diets. However, in vitro SC from excess diets tended to proliferate 13.7% (P = 0.08) less than SC from adequate diets, with deficient diets being intermediate and not different from the other 2 (P ≥ 0.49). Similarly, myoblast fusion rates were greatest in adequate diets, with deficient diets having 9.2% lower fusion rates (P = 0.05) and excess diets exhibiting 20.7% lower fusion rates than those fed adequate diets (P < 0.001). These data indicate that diets deficient in Ca-PO4 decrease satellite cell activity, which may lead to a reduction in postnatal muscle growth. Additionally, excess dietary Ca-PO4 appears to reduce satellite cell proliferation and differentiation in vitro. Diets adequate in Ca-PO4 have the greatest proliferation and differentiation rates, which may improve the growth potential of the animal. [ABSTRACT FROM AUTHOR]

Dietary calcium and phosphate intake during the neonatal period may be of critical importance for lifetime skeletal development. In older animals, calcium and phosphate homeostasis is orchestrated by intestinal absorption, bone turnover, and kidney excretion, which are regulated by several hormones such as parathyroid hormone (PTH), calcitonin, fibroblast growth factor 23 (FGF23), and calcitriol [1,25(OH)2D3]. In older animals, the PTH/calcitriol system appears to be the major regulator of calcium and phosphate homeostasis; however, in neonates, this system is not fully developed. We hypothesized that dietary calcium and phosphate concentrations would affect the expression of genes involved in calcium and phosphate homeostasis in neonatal pigs. Twenty-seven neonatal pigs (24 ± 6 h old) were randomly assigned into 1 of 3 treatment groups. Groups received a milk replacer diet for 16 d that contained calcium and phosphate at a 25% deficiency, adequate, or 25% excess (NRC standard). At the completion of the feeding trial, samples of the liver and kidney were obtained for total RNA isolation. Gene expression of vitamin D receptor (VDR), parathyroid hormone receptor (PTHR), type II sodium-dependent phosphate cotransporter (NPT2), vitamin D-activating enzyme 1a-hydroxylase (Cyp27B1), and 1,25-dihydroxy vitamin D3-24-hydroxylase (Cyp24A1) were determined by real-time PCR. Data, adjusted by housekeeping gene ribosomal protein L4 (RPL4), were normalized back to the deficient group and then analyzed by ANOVA using the GLIMMIX procedure of SAS 9.4. Both PTHR and NPT2 were significantly higher in the calcium- and phosphate-deficient group than in the adequate group (1.01 ± 0.07 vs. 0.75 ± 0.08 for PTHR and 1.01 ± 0.09 vs. 0.65 ± 0.09 for NPT2; P < 0.05). No significant differences were detected between the excess group and any other 2 groups. Similarly, expression of Cyp27B1 was significantly higher in the deficient group than in both the adequate and excess groups (1.10 ± 0.13 in the deficient group, 0.60 ± 0.13 in the adequate group, and 0.55 ± 0.13 in the excess group). These results provide some clues into the homeostatic regulation of calcium and phosphate in neonates. Based on these results, even a small deficiency in dietary calcium and phosphate intake can initiate transcriptional changes of key regulatory gene pathways to maintain homeostatic conditions. [ABSTRACT FROM AUTHOR]

The costs associated with dietary phosphorus (P) supplementation, as well as public concerns, have driven research towards finding ways to reduce dietary P supplementation to, as well as P excretion from, pigs. Our previous work suggests differences in the regulation of P homeostasis exist between weanling pigs of different genetic backgrounds (Hittmeier et al., 2005). In this study, we examined the impact of genetic background and mild dietary P restriction on growth and bone integrity in 48 gilts sired by two different sire lines (LB and HB). They were fed either a P adequate (PA) or a P deficient (PD) diet over a 14 wk trial. The PD provided 20% less available P than the PA. Plasma phosphorus concentration, ADG, ADFI, and G:F were determined biweekly. At the completion of the trial, radial bones were collected for bone strength analysis and intermediate carpal bones were collected for ash content determination. Data were analyzed using a mixed model with genetic line, diet, and line x diet considered as fixed effects and litter as a random effect. Initial BW and final BW were covariates for growth performance and bone strength, respectively. After 4wk on trial, reduced ADG (P < .05) was seen among LB pigs fed the PD, but not among the HB pigs. The depressed ADG among LB PD pigs corresponded with a lower (P < .05) G:F. These differences were not seen by 14wk. Lower (P < .05) plasma P concentrations in PD fed pigs were seen at wk14. The bones of pigs fed PA were stronger those fed PD (P < .05). Radial bones of HB pigs were more bendable (P < .05) than those of LB pigs, and this increased in both lines with the PD diet (P < .05). Pigs fed the PD had lower (P < .05) breaking strength and ash %. A line*diet effect was also seen in ash %. Among PA fed pigs, LB pigs had higher (P < .05) ash % than HB pigs. These differences suggest that genetic background affects bone integrity and altered regulation of mineral homeostasis between these lines may help explain these differences. Future research could lead to genotype specific dietary P requirements and/or breeding strategies to produce more "environmentally-friendly" pigs. [ABSTRACT FROM AUTHOR]

Escherichia coli infections, causing post-weaning diarrhea or edema disease, are one of the most commonly reported disease problems in young pigs in this country, causing substantial losses to the swine industry due to both mortality and morbidity. With worldwide concern over the use of prophylactic antibiotics in animal agriculture, the development of new products to protect swine from E. coli infections is urgently needed. We have previously shown that Colicin E1 is highly effective against the E. coli strains (F4 and F18) responsible for post-weaning diarrhea and edema disease in pigs. In order to make a colicin product more cost-effective for use in swine diets, we recombinantly expressed Colicin E1 in the yeast Pichia pastoris. The Colicin E1 gene was amplified by PCR and ligated into a yeast expression vector, pPICZαC, under control of the methanol inducible AOX1 promoter. The construct was then chromosomally integrated into P. pastoris X33 by electroporation. Transformants were selected by Zeocin resistance. Both the supernatant and cell extract of the transformed yeast were screened for colicin activity by spot testing onto lawns of E. coli DH5α. Yeasts demonstrating the highest colicin activity were selected for batch fermentation studies. Time course studies demonstrated that maximum Colicin E1 levels were obtained in the cell extract after 4d of methanol induction. No detectable colicin activity was found in the supernatant. The level of expression obtained in the yeast was comparable to that obtained with Mitomycin C induction of the native Colicin E1 producing E. coli, approximately 100U/mL of culture. Expressing an active Colicin E1 as an intracellular protein in P. pastoris is advantageous because both purification and processing costs would be dramatically reduced because the yeast may be directly fed to the piglets post-weaning. The production of Colicin E1 by a yeast system holds promise as an alternative to conventional antibiotics for the treatment/prevention of E. coli disease in pigs. [ABSTRACT FROM AUTHOR]

One hundred forty spring-born Angus × Gelbvieh and purebred Angus steers were selected for study as early weaned (EW; average age at weaning = 90 ± 30 d) or traditionally: weaned (TW; average age at weaning = 174 ± 37 d) steers that were nonimplanted or implanted (Synovex-S, Fort Dodge Animal Health, Overland Park, KS). Initially, steers were sorted by age, sire, and farm, and then allotted randomly in a 2 × 2 factorial arrangement of treatments of EW implanted (EWI), EW nonimplanted (EWN), TW implanted (TWI), or TW nonimplanted (TWN). Ultrasound measurements (US) of LM area (LMA), 12th rib fat thickness (US-BF), and marbling (US-M) were collected every 28 d during the time that steers were on feed. At 202 d of age, EW calves had larger US-LMA, US-BF, and BW than TW calves (37.9 vs. 32.3 cm², 0.38 vs. 0.26 cm, and 271.6 vs. 218.9 kg, respectively; P < 0.001). At slaughter, EW calves had heavier HCW (290.4 vs. 279.7 kg, respectively; P < 0.05) and greater USDA marbling scores (51.25 vs. 46.26, respectively; P < 0.05) than TW calves; more EW steers graded USDA Choice or greater (P = 0.05). However, no differences were detected in BW (P = 0.15), LMA (P = 0.39), BF (P = 0.45), or liver abscess scores (P = 0.41). Twenty-four implanted steers were selected from the original group of 140 and sorted into two slaughter groups of 12. Twelve implanted steers from each weaning group, matched in slaughter BW but differing in age, were subsampled at slaughter to assess the effect of weaning age and chronological age on muscle tenderness. Younger animals had lower Warner-Bratzler shear force values (P < 0.001) than older calves after 14 d of postmortem aging; however, no differences were found in tenderness after 21 d of aging. Furthermore, there was greater variance (P < 0.001) in Warner-Bratzler shear force values among younger, EW steers vs. older, TW steers. These data provide evidence that early weaning of beef calves may be used as a tool to more effectively manage the cow-calf production system without compromising the quality of the offspring. [ABSTRACT FROM AUTHOR]