Kyphosis is an idiopathic disease characterized by abnormal, outward spinal curvature. A spontaneous outbreak and subsidence of kyphosis over a 4-mo period in the University of Wisconsin Swine Research and Teaching Center herd coincided with an accidental omission of vitamin D₃ in 1 of 2 premixes used in sow diets. This controlled experiment was conducted to determine whether vitamin D deletion from premixes used in sow diets would induce kyphosis in their offspring. Crossbred (Landrace × Large White), multiparous sows (n = 8) were fed corn–soybean meal diets supplemented with either 325 IU vitamin D₃/kg (+D) or 45 IU vitamin D₃/kg (–D) diet from breeding through lactation. The vitamin D concentrations duplicated formulations of diets fed during the earlier spontaneous outbreak. At weaning (approximately 4 wk), pigs were fed diets devoid of supplemental vitamin D and formulated to supply either 120% of the Ca and P requirements (HCaP) or 80% of the Ca and P requirements (LCaP) until wk 9. At wk 9, all pigs were fed the HCaP diet until wk 13. No evidence of kyphosis was observed in pigs at weaning. Pigs produced by –D sows and fed LCaP diets exhibited a 17% incidence (4/23 pigs) of kyphosis at wk 9. At wk 13, the incidence of kyphosis had increased to 32% (6/19 pigs). Unexpectedly at wk 13, pigs produced by +D sows and fed LCaP diets exhibited a 26% incidence (5/19 pigs) of kyphosis. None of the pigs fed HCaP diets from wk 4 to 13 displayed kyphosis, regardless of maternal diets. Evidence of kyphosis was detected at a younger age if pigs were produced by sows fed –D diets. Whole body and femur bone mineral content determined with dual energy X-ray absorptiometry were reduced (P < 0.05) in pigs fed LCaP vs. HCaP diets, but pigs produced by –D sows were more severely affected. Femur bending moments were reduced (P < 0.05) at wk 9 and 13 in pigs fed LCaP vs. HCaP diets. At wk 13, pigs produced by –D sows and fed LCaP diets had reduced (P < 0.05) bone mineral density and femur yield bending moment compared with pigs from +D sows fed LCaP diets. In conclusion, the 20 to 30% incidence of kyphosis induced by altering vitamin D, Ca, and P concentrations in maternal and nursery diets mimics the incidence observed in spontaneous outbreaks in afflicted herds. A reproducible vitamin D-induced kyphosis in young pigs offers a suitable model to study skeletal tissue characteristics, fetal skeletal tissue development, and potential treatments for pigs and human patients afflicted by this disease. Copyright © 2013. American Society of Animal Science .

Systemic factors that ultimately affect skeletal growth involve interrelationships among Ca, parathyroid hormone (PTH), and conversion of 25-OH vitamin D₃ to the active hormone, 1α,25-(OH)₂D₃. These interrelationships, with a focus on mechanisms that affect Ca homeostasis, are referred to as the Ca, PTH, and vitamin D axis. Relatively little research has focused on these interrelationships and P homeostasis. In the past decade, discovery of a previously unrecognized hormone involved in a pathway for P homeostasis offers opportunities to improve P efficiency without compromising skeletal growth and animal well-being. The objective of this review was to summarize pivotal research discoveries that led to the current understanding of the roles of fibroblast growth factor 23 (FGF23) in P homeostasis that are independent from the well-described pathways involved with Ca homeostasis. The novel pathways are referred to as the FGF23, P, and vitamin D axis. The peptide, FGF23, directly affects P homeostasis via action on renal target tissues to regulate Na-P transport proteins and renal 25(OH)D₃-1α hydroxylase activity. Identification of bone as the primary site for FGF23 production ascribes an endocrine gland function to bone. Within 9 h after a single injection of recombinant FGF23, mice displayed hypophosphatemia and urinary P wasting. In contrast, FGF23 knockout mice displayed hyperphosphatemia and renal P conservation. These responses were independent of PTH. Applications of the FGF23, P, and vitamin D axis in dietary strategies for animal agriculture need to be explored. Development of dietary inputs to balance both Ca and P homeostasis are needed to improve skeletal growth and nutrient efficiency. Copyright © 2011. American Society of Animal Science .

Background: The purpose of this study was to explore the role of perinatal vitamin-D intake on the development and characterization of hyperkyphosis in a porcine model. Methods: The spines of 16 pigs were assessed at 9, 13, and 17 weeks of age with radiography and at 17 weeks with computed tomography (CT), magnetic resonance imaging (MRI), histology, and bone-density testing. An additional 169 pigs exposed to 1 of 3 maternal dietary vitamin-D levels from conception through the entire lactation period were fed 1 of 4 nursery diets supplying different levels of vitamin D, calcium, and phosphorus. When the animals were 13 weeks of age, upright lateral spinal radiography was performed with use of a custom porcine lift and sagittal Cobb angles were measured in triplicate to determine the degree of kyphosis in each pig. Results: The experimental animals had significantly greater kyphotic sagittal Cobb angles at all time points when compared with the control animals. These hyperkyphotic deformities demonstrated no significant differences in Hounsfield units, contained a slightly lower ash content (46.7% ± 1.1% compared with 50.9% ± 1.6%; p < 0.001), and demonstrated more physeal irregularities. Linear mixed model analysis of the measured kyphosis demonstrated that maternal diet had a greater effect on sagittal Cobb angle than did nursery diet and that postnatal supplementation did not completely eliminate the risk of hyperkyphosis. Conclusions: Maternal diets deficient in vitamin D increased the development of hyperkyphosis in offspring in this model. Clinical Relevance: This study demonstrates that decreased maternal dietary vitamin-D intake during pregnancy increases the risk of spinal deformity in offspring. In addition, these data show the feasibility of generating a large-animal spinal-deformity model through dietary manipulation alone.

Despite two extensive reprogramming events during early embryogenesis and gametogenesis, epigenetic information can be passed to the next generations, which constitutes the transgenerational epigenetic inheritance of phenotypes. Considering its utmost importance, there have been few studies focused on the transgenerational effects of dietary interventions, such as methionine supplementation, in livestock. Using whole-genome bisulfite sequencing, we implemented a single-base resolution differential methylation analysis for the F3 and F4 descendants of control vs. methionine-supplemented F0 twin-pair rams. Based on the results of our previous study on F0, F1, and F2 generations, we compared current results of 2981 and 1726 differentially methylated cytosines (DMCs), as well as 798 and 553 unique differentially methylated genes (DMGs), in F3 and F4, respectively. We identified 41 DMGs that exhibited transgenerational epigenetic inheritance (TEI-DMGs) across four generations and 11 TEI-DMGs across five generations. Finally, we estimated the effect size of F0 diet group on F3 and F4 growth and fertility-related phenotypes, providing evidence for transgenerational effects of diet group accompanying inherited differentially methylated genes. Here, for the first time using gene-level and phenotypic data, we demonstrate that a moderate dietary intervention can exert long-lasting transgenerational effects on offspring phenotypes extending beyond the F2 generation in sheep.

Phosphorus requirements of reproducing sows were estimated using 24-h urinary P excretion. Thirty-six multiparous sows were fed one of six maize–soybean meal-based diets with total P ranging from 0·40 to 0·80 % in 0·08 % increments with a constant Ca:total P ratio (1·25:1). Diets were fed from day 7·5 ± 1 after breeding until the end of lactation (day 26 ± 1). Urine samples were collected in mid and late gestation (days 77·1 ± 2 and 112·4 ± 1) and early and late lactation (days 4·5 ± 1 and 18·2 ± 1). Phosphorus requirements were estimated using linear and nonlinear regression models. Based on a single 24-h urinary P excretion, estimated daily dietary total P requirements in mid and late gestation were 10·3 g (6·0 g standardised total tract digestible P, STTD P), and estimates for early and late lactation were 31·1 g (16·6 g STTD P) and 40·3 g (22·1 g STTD P), respectively. Plasma P and Ca concentrations were maintained within normal ranges at the estimated levels of P requirements. No differences among treatments were observed for plasma parathyroid hormone (P ≥ 0·06) and bone formation marker (P ≥ 0·16). In lactation, bone resorption marker decreased (P ≤ 0·001) as sows consumed more P. Among the analysed variables, urinary P was the most sensitive response to changes in dietary P intake. Urinary P excretion offers a practical method to estimate P requirements in sows. Our recommended daily total P requirements are 10·3 g for gestation and 35·7 g for lactation.

Limited evidence is available to validate beneficial responses from extra nutrient supplements for mediation of growth suppression that results from immune challenges. Extrarenal roles of vitamin D metabolites in immune function implicate vitamin D₃ supplements as a nutrient for potential beneficial effects. The current objective was to assess growth and bone ash responses to dietary vitamin D₃ (D) supplements for growing pigs undergoing an immune challenge. At weaning, 216 crossbred pigs (4 pigs/pen, 6 pens/treatment) were randomly allotted within sex and weight blocks to 1 of the 9 treatments. Treatments included D supplements (0, 100, or 800 IU/kg) in a factorial arrangement with 3 vaccine (V) protocols; no injection (0 × V), a single 2 mL injection of a Lawsonia intracellularis vaccine at day 14 (1 × V), or 2 mL injections of the same vaccine at days 0 and 7 (2 × V). An adjustment diet with no supplemental D was fed for 1 wk, then assigned D diets for 2 wk (P2). After P2, all pigs were phase-fed standard diets (D = 280 IU/kg) to assess subsequent growth to 115 kg. No differences due to D supplements or vaccination protocol were detected in ADG (0.233 ± 0.021 kg/d) or GF (0.642 ± 0.028 kg/d) over the 21-d nursery trial; however, ADFI was lower (P < 0.10) in pigs fed D levels of 0 vs. 100 and 800 (0.340 vs. 0.375, 0.372 ± 0.027 kg/d). Bone mineral content (g) from whole-body dual energy X-ray absorptiometry scans at 9 wk (n = 4 pigs/treatment) was lower in pigs fed 0 vs. 100 and 800 IU of D (287 vs. 325, 323 ± 34.1 g/pig). Growth from nursery to 115 kg was lower (P < 0.01) in pigs fed D levels of 0 vs.100 and 800 (0.828 vs. 0.876, 0.889 ± 0.021 kg/d). At market, approximately two-thirds of pigs showed positive L. intracellularis serology titers regardless of treatment. Limited evidence for D-mediation of an immune challenge using the vaccination protocols may be a consequence of limited vaccine effects on growth in the nursery and seroconversion of most pigs to L. intracellularis by market.