Concern over the environmental impact of phosphate (P) excretion from pig production has led to reduced dietary P supplementation to these animals. These reductions may cause minor dietary P deficiency, a problem also seen in segments of the human populace. To examine how genetics influences P utilization, ninety-four gilts sired by two different genetic lines (PIC337 and PIC280) were fed either a P adequate diet or a 20% P deficient diet for 14 wk. Blood samples were collected and BW recorded monthly following an overnight fast. Upon completion of the study, radial bones with attached ulnae, intermediate carpals, and kidney tissue samples were collected. After 12 wk on the experimental diets, an additional 28 pigs (approximately 100 kg BW) produced by the same breeding strategy as described above, were moved into individual stainless steel metabolism crates (1.2 m x 2.4 m). Twice daily, feces and urine were collected from each metabolism crate for P balance analysis. Dietary treatment, sire, and their interaction significantly affected plasma 1, 25 (OH) 2 vitamin D and PTH concentrations, growth performance, bone strength, and gene expression in the kidney. The PIC337 sired pigs consumed more feed and gained more weight than their PIC280 sired counterparts (P 0.05). Regardless of sire line, pigs fed the P deficient diet had lower (P 0.05) plasma P concentrations and were less efficient at converting feed to BW (P 0.05). The P deficient pigs had increased (P 0.05) plasma concentrations of 1, 25 (OH)2 vitamin D and decreased concentrations of PTH after 4 wk. While plasma 1, 25 (OH)2 vitamin D concentrations were elevated (P 0.05) in all the P deficient animals, this increase was larger among the PIC337 sired pigs. As expected, P deficiency resulted in weaker bones with lower percent ash (P 0.05). Among the P adequate pigs, the bones of PIC337 sired pigs were stronger (P 0.05) and had higher (P 0.05) ash percentage compared to PIC280 sired pigs. Increased (P 0.05) levels of the CYP27B1 and PTHR mRNA were seen in P deficient pigs. Those animals housed in metabolism crates fed the P deficient diet had lower dietary P intakes, as well as lower fecal P excretion compared to pigs fed the P adequate diet (P 0.01), though there were no significant differences based on sire line or the interaction of sire line and dietary P in any of the P balance indices measured. These data suggest differing mechanisms of regulation of P utilization between these genetic lines.;In order to examine the impact of a single nucleotide polymorphism in the calcitonin receptor gene (CALCR) previously shown to be associated with bone integrity on P utilization in growing pigs, forty-two gilts were fed either a P adequate diet or a 20% P deficient diet for 14 wk. Plasma P concentrations of animals receiving the adequate diet were higher than their deficient counterparts at 8 wk and subsequent samplings until trial completion (P 0.05). P adequacy also resulted in increased concentrations of 1, 25 (OH)2 vitamin D and decreased PTH concentrations at 8 wk (P 0.05). P deficiency reduced bone strength and mineral content, regardless of genotype (P 0.05). Among pigs fed the P adequate diet, the 11 and 22 genotypes had higher bone modulus and ash percentage compared to their P deficient counterparts (P 0.05). However, these differences were not observed within animals having the 22 genotype. Neither dietary treatment nor CALCR genotype effected growth performance. These data suggest that this CALCR SNP is associated with the regulation of P utilization. Elucidating the genetic mechanisms responsible for P utilization would have important implications to for both animal and human health.
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