0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      A review of calcium and phosphorus requirement estimates for gestating and lactating sows

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Calcium (Ca) and phosphorus (P) are minerals involved in biological functions and essential structural components of the skeleton. The body tightly regulates Ca and P to maintain homeostasis. Maternal needs for Ca and P increase during gestation and lactation to support conceptus growth and milk synthesis. Litter size and litter average daily gain (ADG) have a large effect on Ca and P requirements for sows because as they increase, the requirements increase due to a greater need from the sow. The objective of this review was to summarize published literature on Ca and P requirements in gestating and lactating sows derived from empirical data and factorial models. A total of nine empirical studies and seven factorial models were reviewed for determining the Ca and P requirements in gestation. For lactation, there were six empirical studies and seven factorial models reviewed. Empirical studies determined requirements based on the observed effect of Ca and P on bone mineralization, sow and litter performance, and milk characteristics. Factorial models generated equations to estimate Ca and P requirements using the main components of maintenance, fetal and placental growth, and maternal retention in gestation. The main components for factorial equations in lactation include maintenance and milk production. In gestation, the standardized total tract digestible phosphorus (STTD P) requirement estimates from empirical studies range from 5.4 to 9.5 g/d with total Ca ranging from 12.9 to 18.6 g/d to maximize bone measurements or performance criteria. According to the factorial models, the requirements increase throughout gestation to meet the needs of the growing fetuses and range from 7.6 to 10.6 g/d and 18.4 to 38.2 g/d of STTD P and total Ca, respectively, on day 114 of gestation for parity 1 sows. During lactation, STTD P requirement estimates from empirical studies ranged from 8.5 to 22.1 g/d and total Ca ranged from 21.2 to 50.4 g/d. For the lactation factorial models, STTD P requirements ranged from 14.2 to 25.1 g/d for STTD P and 28.4 to 55.6 g/d for total Ca for parity 1 sows with a litter size of 15 pigs. The large variation in requirement estimates makes it difficult to define Ca and P requirements; however, a minimum level of 6.0 and 22.1 g/d of STTD P during gestation and lactation, respectively, appears to be adequate to meet basal requirements. The limited data and high variation indicate a need for future research evaluating Ca and P requirements for gestating and lactating sows.

          Abstract

          Dietary supply of Ca and P during gestation and lactation is important to ensure adequate skeletal growth and development. This review summarizes available data reporting requirement estimates of Ca and P for gestating and lactating sows.

          Related collections

          Most cited references89

          • Record: found
          • Abstract: found
          • Article: not found

          FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis.

          We analyzed the effects of an FGF-23 injection in vivo. FGF-23 caused a reduction in serum 1,25-dihydroxyvitamin D by altering the expressions of key enzymes for the vitamin D metabolism followed by hypophosphatemia. This study indicates that FGF-23 is a potent regulator of the vitamin D and phosphate metabolism. The pathophysiological contribution of FGF-23 in hypophosphatemic diseases was supported by animal studies in which the long-term administration of recombinant fibroblast growth factor-23 reproduced hypophosphatemic rickets with a low serum 1,25-dihydroxyvitamin D [1,25(OH)2D] level. However, there is no clear understanding of how FGF-23 causes these changes. To elucidate the molecular mechanisms of the FGF-23 function, we investigated the short-term effects of a single administration of recombinant FGF-23 in normal and parathyroidectmized animals. An injection of recombinant FGF-23 caused a reduction in serum phosphate and 1,25(OH)2D levels. A decrease in serum phosphate was first observed 9 h after the injection and was accompanied with a reduction in renal mRNA and protein levels for the type IIa sodium-phosphate cotransporter (NaPi-2a). There was no increase in the parathyroid hormone (PTH) level throughout the experiment, and hypophosphatemia was reproduced by FGF-23 in parathyroidectomized rats. Before this hypophosphatemic effect, the serum 1,25(OH)2D level had already descended at 3 h and reached the nadir 9 h after the administration. FGF-23 reduced renal mRNA for 25-hydroxyvitamin D-1alpha-hydroxylase and increased that for 25-hydroxyvitamin D-24-hydroxylase starting at 1 h. In addition, an injection of calcitriol into normal mice increased the serum FGF-23 level within 4 h. FGF-23 regulates NaPi-2a independently of PTH and the serum 1,25(OH)2D level by controlling renal expressions of key enzymes of the vitamin D metabolism. In conclusion, FGF-23 is a potent regulator of phosphate and vitamin D homeostasis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The bone remodelling cycle.

            The bone remodelling cycle replaces old and damaged bone and is a highly regulated, lifelong process essential for preserving bone integrity and maintaining mineral homeostasis. During the bone remodelling cycle, osteoclastic resorption is tightly coupled to osteoblastic bone formation. The remodelling cycle occurs within the basic multicellular unit and comprises five co-ordinated steps; activation, resorption, reversal, formation and termination. These steps occur simultaneously but asynchronously at multiple different locations within the skeleton. Study of rare human bone disease and animal models have helped to elucidate the cellular and molecular mechanisms that regulate the bone remodelling cycle. The key signalling pathways controlling osteoclastic bone resorption and osteoblastic bone formation are receptor activator of nuclear factor-κB (RANK)/RANK ligand/osteoprotegerin and canonical Wnt signalling. Cytokines, growth factors and prostaglandins act as paracrine regulators of the cycle, whereas endocrine regulators include parathyroid hormone, vitamin D, calcitonin, growth hormone, glucocorticoids, sex hormones, and thyroid hormone. Disruption of the bone remodelling cycle and any resulting imbalance between bone resorption and formation leads to metabolic bone disease, most commonly osteoporosis. The advances in understanding the cellular and molecular mechanisms underlying bone remodelling have also provided targets for pharmacological interventions which include antiresorptive and anabolic therapies. This review will describe the remodelling process and its regulation, discuss osteoporosis and summarize the commonest pharmacological interventions used in its management.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Parathyroid hormone: anabolic and catabolic actions on the skeleton.

              Parathyroid hormone (PTH) is essential for the maintenance of calcium homeostasis through, in part, its actions to regulate bone remodeling. While PTH stimulates both bone formation and bone resorption, the duration and periodicity of exposure to PTH governs the net effect on bone mass, that is whether it is catabolic or anabolic. PTH receptor signaling in osteoblasts and osteocytes can increase the RANKL/OPG ratio, increasing both osteoclast recruitment and osteoclast activity, and thereby stimulating bone resorption. In contrast, PTH-induced bone formation is explained, at least in part, by its ability to downregulate SOST/sclerostin expression in osteocytes, permitting the anabolic Wnt signaling pathway to proceed. The two modes of administration of PTH, that is, continuous vs. intermittent, can regulate, in bone cells, different sets of genes; alternatively, the same sets of genes exposed to PTH in sustained vs. transient way, will favor bone resorption or bone formation, respectively. This article reviews the effects of PTH on bone cells that lead to these dual catabolic and anabolic actions on the skeleton.
                Bookmark

                Author and article information

                Contributors
                Journal
                Transl Anim Sci
                Transl Anim Sci
                tranas
                Translational Animal Science
                Oxford University Press (US )
                2573-2102
                2024
                23 May 2024
                23 May 2024
                : 8
                : txae087
                Affiliations
                Department of Animal Sciences and Industry, College of Agriculture, Kansas State University , Manhattan, KS, USA
                Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University , Manhattan, KS, USA
                Department of Animal Sciences and Industry, College of Agriculture, Kansas State University , Manhattan, KS, USA
                Department of Animal Sciences and Industry, College of Agriculture, Kansas State University , Manhattan, KS, USA
                Department of Animal Sciences and Industry, College of Agriculture, Kansas State University , Manhattan, KS, USA
                Department of Animal Sciences and Industry, College of Agriculture, Kansas State University , Manhattan, KS, USA
                Author notes
                Corresponding author: goodband@ 123456ksu.edu
                Author information
                https://orcid.org/0000-0001-7268-4278
                Article
                txae087
                10.1093/tas/txae087
                11165643
                38863597
                fae6e0b1-39d3-4634-9291-811716404df7
                © The Author(s) 2024. Published by Oxford University Press on behalf of the American Society of Animal Science.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.

                History
                : 22 March 2024
                : 22 May 2024
                : 11 June 2024
                Page count
                Pages: 22
                Categories
                Non Ruminant Nutrition
                AcademicSubjects/SCI00960

                calcium,gestation,lactation,phosphorus,sow
                calcium, gestation, lactation, phosphorus, sow

                Comments

                Comment on this article