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Metabolism of vitamin D, Calcium and Phosphorus and their disorders in goats

The review article presents materials on the metabolism of the mostcommon vitamins of group D ergocalciferol (D2), cholecalciferol (D3), aswell as essential macronutrients Ca and Phosphorus and their disorders ingoats. Since the primary forms of vitamin D (D2 and D3) are biologicallyinactive and must undergo several stages of hydroxylation to be activated,the biological role and importance for the body of active metabolites ofvitamin D3 25OH D3 (synthesised mainly in the liver under the influenceof hepatic cytochromes P450) and 1, 25(OH)2 D3 and 24,25(OH)2 D3 (theirsynthesis occurs via 1α-hydroxylase in the mitochondria of proximal cellsof the convoluted tubules of the kidneys).It is believed that the liver, while playing an important role in themetabolism of vitamin D and its metabolites and producing 25OH D3, isalso the only organ that synthesises DBP, which transports 25OH D3 totissues and maintains its concentration in the circulatory system.Vitamin D becomes biologically active only after the second stageof hydroxylation is completed. Renal 1α-hydroxylase (CYP27B1),regulated by parathyroid hormone (PTH), plays an important role inthe transformation of the extracellular substrate 25OH D3 to 1,25(OH)2D3, which exerts its effect on target cells and tissues by binding to thenuclear vitamin D receptor. Alternatively, 1,25(OH)2 D3 can bind to theplasma membrane VDR and induce non-genomic actions, in particular,stimulation of intestinal calcium transport.Vitamin D is a steroid substance that is essential for all vertebratesto maintain calcium and phosphorus metabolism within optimal limits, ahealthy skeleton, muscle contraction, modulation of cell growth and neuromuscular function. Calciferol also regulates the immune system, inhibits the development of pathological cells, angiogenesis and inflammatoryreactions. The active form of vitamin D, 1,25(OH)2 D3, stimulates intestinal absorption and renal Ca reabsorption and maintains its minimumphysiological level in the blood.Vitamin D deficiency in goats leads to a decrease in productivity, causesa decrease in intestinal and renal calcium reabsorption, which leads to theincrease in parathyroid hormone levels. This process leads to activation ofosteocytes and, as a result, accelerates bone demineralisation, causing thedevelopment of many diseases in adults, including nutritional and fibrousosteodystrophy, secondary osteodystrophy, endocrine dysfunction), as wellas rickets in young animals. The development of non-skeletal pathologies,in particular, inflammatory, neoplastic and autoimmune diseases, is also associated with cholecalciferol deficiency in the body. In addition, disordersof D-vitamin and calcium-phosphorus metabolism in goats cause the development of postpartum hypocalcaemia and postpartum hypophosphatemia.In the animal body, calcium and phosphorus homeostasis is maintained by a coordinated interaction of absorption and reabsorptionthrough the gastrointestinal tract and kidneys, as well as by storage and mobilization from bone tissue and is regulated mainly by biologically active cholecalciferol metabolites - 25OH D3, 1,25(OH)2 D3, as wellas parathyroid hormone (PTH; synthesised by the pineal glands) andcalcitonin (CT; produced by sparafollicular (light) thyroid C cells) andfibroblast growth factor-23 (FGF23).In contrast to monogastric animals, small ruminants do not modulaterenal calcium excretion in response to calcium limitation in the diet. Themobilization of Ca and P from the skeleton is stimulated by PTH throughosteoclast activation mediated by receptor activator of nuclear factor-κB(RANK). Vitamin D maintains Ca (by stimulating CaZB) and P homeostasis (the direct rapid action of 1,25(OH)2 D3 has been proven to have a directeffect on the absorption of these vital elements in the intestine, reabsorptionof these cations in the renal tubules and their mobilization from bone tissue).Phosphorus is a component of adenosine triphosphate (ATP) and nucleotides. Macroergic phosphate compounds, among which the main oneis adenosine triphosphate acid, provide both the accumulation of energyreserves and its consumption (ATP, ADP, creatine phosphate), affectingprotein, lipid, carbohydrate, mineral, and energy metabolism. An interaction between vitamin D and fibroblast growth factor 23 (FGF23), a bonehormone that causes the development of phosphaturia and reduces thesynthesis of 1,25(OH)2 D3, has been identified.Despite the multidirectionality of etiological factors, common to allforms of osteodystrophy is a disruption of the processes of bone formation and renewal, which is manifested by increased mobilization of calcium, phosphorus and other elements from bone tissue, so the pathologyis accompanied by osteomalacia, osteoporosis and osteofibrosis, and aviolation of the mechanism of maintaining their homeostasis.The main factors of osteodystrophy in animals are feeding disordersand physical inactivity, and the leading links in its pathogenesis are theimbalance between bone formation and resorption.The main methods for diagnosing disorders of D-vitamin and calcium-phosphorus metabolism in goats are clinical, physical, biochemical,enzyme-linked immunosorbent assays and pathological and morphological studies. Biochemical analysis in goat serum determines the content oftotal calcium, inorganic phosphorus, activity of alkaline phosphatase andits isozymes, and immunoassay the concentration of 25OH D3, 1,25(OH)2D3, calcitonin and parathyroid hormone.

Keywords: goats, vitamin D, metabolites, metabolism, calcium,phosphorus, liver, kidneys.

SAKHNYUK V. https://orcid.org/ 0000-0002-3070-9876


HOTSULIAK M. https://orcid.org/0009-0004-6165-5032


  1. Fleet, James C. (2017). The role of vitamin Din the endocrinology controlling calcium homeostasis.Molecular and cellular endocrinology. Vol. 453, pp.36–45. DOI:10.1016/j.mce. 2017.04.008.
  2. Young, M. F. (2023). Assessment of VitaminD status and association with inflammation: Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRINDA) project. The Amer ican Journal of Clinical Nutrition. DOI:10.1016/j.ajcnut.2022.10.018.
  3. Nair, R., Maseeh, A. (2012). Vitamin D:The “sunshine” vitamin. Journal of phamacology and pharmacotherapeutics, Vol. 3 (2), pp. 118–126. Available at:journals.sagepub.com/ doi/pdf/10.4103/0976-500X.95506.
  4. Handel, I. (2016). Vitamin D status predicts reproductive fitness in a wild sheep population. Scientific Reports. Vol. 6, no. 1. DOI:10.1038/srep18986.
  5. Aranow, C. (2011). Vitamin D and the immunesystem. Journal of investigative medicine, Vol. 59 (6),pp. 881–886. DOI:10.2310/JIM.0b013e31821b8.
  6. Lee, S. (2023). 24,25-Dihydroxy Vitamin Dand Vitamin D Metabolite Ratio as Biomarkers of Vitamin D in Chronic Kidney Disease. Nutrients. Vol.15, no. 3, 578 p. DOI:10.3390/ nu15030578.
  7. Bayoumi, Y. H. (2021). Peri-parturient hypocalcemia in goats: Clinical, hematobiochemical profiles and ultrasonographic measurements of postpartum uterine involution. Vol. 14, no. 3, pp. 558–568.DOI:10.14202/vetworld.2021.558-568.
  8. Wild, K. J. (2021). Meta-analysis-based estimates of efficiency of calcium utilisation by ruminants. Vol. 15, no. 8, 100315 p. DOI:10.1016/j.animal.2021.100315.
  9. Mi, H. (2022). Calcium Homeostasis and BoneMetabolism in Goats Fed a Low Protein Diet. Frontiers in Veterinary Science. Vol. 8. DOI:10.3389/fvets.2021.829872.
  10. Brozos, C., Mavrogianni, V. S., Fthenakis, G. C.(2011). Treatment and Control of Peri-Parturient Metabolic Diseases: Pregnancy Toxemia, Hypocalcemia,Hypomagnesemia. Veterinary Clinics of North America: Food Animal Practice. Vol. 27, no. 1, pp. 105–113.DOI:10.1016/ j.cvfa.2010.10.004.
  11. Grünberg, W. (2014). Treatment of Phosphorus Balance Disorders. Veterinary Clinics of NorthAmerica: Food Animal Practice. Vol. 30, no. 2,pp. 383–408. DOI:10.1016/j.cvfa. 2014.03.002.
  12. Sidler-Lauff, K. (2010). Influence of differentcalcium supplies and a single vitamin D injection onvitamin D receptor and calbindin D9k immunoreactivities in the gastrointestinal tract of goat kids. Journalof Animal Science, Vol. 88, no. 11, pp. 3598–3610.DOI:10.2527/jas.2009-2682.
  13. Gupta, S. (2018). Systematic Review ofthe Literature: Best Practices. Academic Radiology. Vol. 25, no. 11, pp. 1481–1490. DOI:10.1016/j.acra.2018.04.025.
  14. Amrein, K. (2020). Vitamin D deficiency 2.0:an update on the current status worldwide. European Journal of Clinical Nutrition, Vol. 74, no. 11, pp.1498–1513. DOI:10.1038/s41430-020-0558-y.
  15. Holick, M. F. (2017). The vitamin D deficiency pandemic: Approaches for diagnosis, treatmentand prevention. Reviews in Endocrine and MetabolicDisorders. Vol. 18, no. 2, pp. 153–165. DOI:10.1007/s11154-017-9424-1.
  16. Madan, J., Sindhu, S., Rose, M. K. (2020).Changes in plasma biochemical parameters and hormones during transition period in Beetal goats carrying single and twin fetus. Vol. 13, no. 6, pp. 1025–1029. DOI:10.14202/vetworld.2020.1025–1029.
  17. Kohler, M. (2013). Influence of altitude on vitamin D and bone metabolism of lactating sheep andgoats. Journal of Animal Science, Vol. 91, no. 11, pp.5259–5268. DOI:10.2527/jas.2013-6702.
  18. Nemeth, M. V., Wilkens, M. R., Liesegang, A.(2017). Vitamin D status in growing dairy goatsand sheep: Influence of ultraviolet B radiation onbone metabolism and calcium homeostasis. Journalof Dairy Science, Vol. 100, no. 10, pp. 8072–8086.DOI:10.3168/jds.2017-13061.
  19. Cortese, F. (2022). Vitamin D and cardiovascular disease risk. A literature overview. MolecularBiology Reports. DOI:10.1007/s11033-022-07373-6.
  20. Walters, M. R. (1992) Newly Identified Actions of the Vitamin D Endocrine System. EndocrineReviews. Vol. 13, no. 4, pp. 719–764. DOI:10.1210/edrv-13-4-719.
  21. Holick, M. F. (2011). Evaluation, Treatment,and Prevention of Vitamin D Deficiency: an EndocrineSociety Clinical Practice Guideline. The Journal ofClinical Endocrinology & Metabolism, Vol. 96, no. 7,pp. 1911–1930. DOI:10.1210/jc.2011-0385.
  22. Al Mheid, I., Quyyumi, A. A. (2017). VitaminD and Cardiovascular Disease. Journal of the American College of Cardiology, Vol. 70, no. 1, pp. 89–100.DOI:10.1016/j.jacc.2017.05.031.
  23. Del, Valle. (2011). Dietary Reference Intakesfor Calcium and Vitamin D / Committee to ReviewDietary Reference Intakes for Vitamin D and Calcium. National Academies Press. Available at:ncbi.nlm.nih.gov/books/NBK56070/pdf/Bookshelf_NBK56070.pdf.
  24. Sagar, S. (2023). Evaluation Of Antioxidantand Anti-Inflammatory Effects Of 1,25 Dihydroxycholecalciferol Formulation- An Invitro Study. Journal ofPopulation Therapeutics and Clinical Pharmacology,Vol. 30, no. 16. DOI:10.47750/jptcp.2023.30.10.029.
  25. Gardner, D. G., Chen, S., Glenn, D. J. (2013).Vitamin D and the heart. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 305, no. 9, pp. 969–977. DOI:10.1152/ajpregu.00322.2013.
  26. Kovács, S., Wilkens, M. R., Liesegang, A.(2015). Influence of UVB exposure on the vitamin Dstatus and calcium homoeostasis of growing sheepand goats. Journal of Animal Physiology and AnimalNutrition, Vol. 99, pp. 1–12. DOI:10.1111/jpn.12311.
  27. Dittmer, K. E., Thompson, K. G. (2010). Vitamin D Metabolism and Rickets in Domestic Animals.Veterinary Pathology. Vol. 48, no. 2, pp. 389–407.DOI:10.1177/0300985810375240.
  28. Zhu, J., DeLuca, H. F. (2012). Vitamin D25-hydroxylase – Four decades of searching, are we there yet?. Archives of Biochemistry and Biophysics. Vol. 523, no. 1, pp. 30–36. DOI:10.1016/j.abb.2012.01.013.
  29. Washabau, R. J., Day, M. J. Canine and feline gastroenterology. Elsevier Health Sciences. ISBN143770302X, 9781437703023.2012.
  30. Sirajudeen, S., Shah, I., Menhali, Al. (2019).A narrative role of vitamin D and its receptor: withcurrent evidence on the gastric tissues. Internationaljournal of molecular sciences, Vol. 20 (15), 3832 p.DOI:10.3390/ijms201538.
  31. Jovicic, S., Ignjatovic, S., Majkic-Singh, N.(2012). Biochemistry and metabolism of vitamin D /Biohemija i metabolizam vitamina D. Journal of medical biochemistry, Vol. 31 (4), 309 p. DOI:10.2478/v10011-012-0028-8.
  32. Okano, T. (2015). The role of the liver in vitamin D metabolism. Clinical calcium, Vol. 25 (11), pp.1613–1618. Available at:clica151116131618. PMID:26503864.
  33. Barragan, M., Good, M., Kolls, J.K. (2015).Regulation of Dendritic Cell Function by Vitamin D.Nutrients. Vol. 7 (9), pp. 8127–8151. DOI:10.3390/nu7095383.
  34. Zhu, J. G. (2013). CYP2R1 is a major, but notexclusive, contributor to 25-hydroxyvitamin D production in vivo. Proceedings of the National Academy of Sciences. Vol. 110, no. 39, pp. 15650–15655.DOI:10.1073/pnas.1315006110.
  35. Bikle, D. D. (2014). Vitamin D Metabolism,Mechanism of Action, and Clinical Applications.Chemistry and Biology. Vol. 21, no. 3, pp. 319–329.DOI:10.1016/j.chembiol.2013. 12.016.
  36. Grienberger, C., Konnerth, A. (2012). Imaging Calcium in Neurons. Neuron. Vol. 73, no. 5, pp.862–885. DOI:10.1016/j.neuron.2012.02.011.
  37. Yefremov, D.V., Hnoievyj, I. V. (2010). Metabolizm pozhyvnykh rechovyn v orhanizmi vivtsematok pry vykorystanni u ikh hodivli novykh premiksiv[Nutrient metabolism in ewes when using new premixes in their feeding]. Nauk.- tekhn. biul. IT NAANUkrainy [Science and technology Bull. IT of the National Academy of Sciences of Ukraine]. no. 102, pp.270–275. Available at:animal. kharkov.ua/archiv/ntb/NTB102.pdf (in Ukrainian).
  38. Tinker, A., Williams, A. J. (1995). Measuring the length of the pore of the sheep cardiac sarcoplasmic reticulum calcium-release channel usingrelated trimethylammonium ions as molecular calipers. Biophysical Journal, Vol. 68, no. 1, pp. 111–120.DOI:10.1016/S0006-3495(95)80165-7.
  39. Takagi, H., Block, E. (1991). Effects of Various Dietary Cation-Anion Balances on Responseto Experimentally Induced Hypocalcemia in Sheep.Journal of Dairy Science, Vol. 74, no. 12, pp. 4215–4224. DOI:10.3168/jds.S0022-0302(91) 78617-7.
  40. Villalba, J. J., Provenza, F. D., Hall, J. O.(2008). Learned appetites for calcium, phosphorus,and sodium in sheep1,2. Journal of Animal Science,Vol. 86, no. 3, pp. 738–747. DOI:10.2527/ jas.2007-0189.41.
  41. Hotsuliak, M.M., Sakhniuk, V.V. (2023).Deiaki teoretychni i praktychni aspekty D-vitaminnoho ta kal'tsiievo-fosfornoho metabolizmu za promyslovoho utrymannia kiz]: materialy Vseukrains'koinaukovo-praktychnoi konferentsii zdobu-vachiv vyschoi osvity «Molod' – ahrarnij nautsi i vyrobnytstvi»[Some theoretical and practical aspects of D-vitaminand calcium-phosphorus metabolism during the industrial keeping of goats: materials of the All-Ukrainianscientific and practical conference of higher educationgraduates "Youth - agricultural science and production" (April 14, 2023)]. Bila Tserkva, pp. 199–200.Available at:science.btsau.edu.ua/sites/ default/files/tezy/tezy_stud_vet_%2014.04.23.pdf (in Ukrainian).
  42. Köhler, O. M. (2020). Dietary phosphorusrestriction affects bone metabolism, vitamin D metabolism and rumen fermentation traits in sheep.Journal of Animal Physiology and Animal Nutrition.DOI:10.1111/jpn.13449.
  43. Wilkens, M. R., Muscher-Banse, A. S.(2020). Review: Regulation of gastrointestinal andrenal transport of calcium and phosphorus in ruminants. Animal. Vol. 14, pp. 29–43. DOI:10.1017/S1751731119003197.
  44. Keung, L., Perwad, F. (2018). Vitamin D andkidney disease. Bone Reports. Vol. 9, pp. 93–100.DOI:10.1016/j.bonr.2018.07.002.
  45. Kumar, R., Thompson, J. R. (2011). Theregulation of parathyroid hor- mone secretion andsynthesis. Journal of the American Society of Nephrology, Vol. 22, no. 2, pp. 216–224. DOI:10. 1681/ASN.2010020186.
  46. Herm, G. (2015). Renal mechanisms of calcium homeostasis in sheep and goats1. Journal ofAnimal Science, Vol. 93, no. 4, pp. 1608–1621.DOI:10.2527/jas.2014-8450.
  47. Levchenko, V.I., Vlizlo, V.V., Kondrakhin, I.P.(2015). Vnutrishni khvoroby tvaryn [Internal diseasesof animals]. Bila Tserkva, Part 2, 610 p. (in Ukrainian).
  48. Ben-awadh, A. N. (2014). Parathyroid Hormone Receptor Signaling Induces Bone Resorption inthe Adult Skeleton by Directly Regulating the RANKLGene in Osteocytes. Endocrinology. Vol. 155, no. 8,pp. 2797–2809. DOI:10.1210/en.2014-1046.
  49. Taylor, M. S. (2007). Calcium and Phosphorus Metabolism in Jersey and Hol-stein Cows DuringEarly Lactation: dissertation. Available at:http://hdl.handle. net/10919/29118.
  50. Savinkov, A. (2020). Effectiveness of the useof complex biological and mineral compounds in alimentary osteodystrophy of lactating cows. BIO Webof Conferences. Vol. 17, 00141. DOI:10.1051/bioconf/20201700141.
  51. Maslak, Yu.V. (2011). Alimentarna osteodystrofiia kiz: patohenez, diahnostyka i likuvannia: avtoref. dys. … kand. vet. nauk: 16.00.01. [Nutritional osteodystrophy of goats: pathogenesis, diagnosis and treatment:abstract of the dissertation of the candidate of veterinarysciences: 16.00.01.] Bila Tserkva. (in Ukrainian).
  52. Handel, I. (2016). Vitamin D status predictsreproductive fitness in a wild sheep population. Scientific Reports. Vol. 6, no. 1. DOI:10.1038/srep18986.
  53. Zhou, P. (2019). Investigation of relationshipbetween vitamin D status and reproductive fitness inScottish hill sheep. Scientific Reports. Vol. 9, no. 1.DOI:10.1038/s41598-018-37843-6.
  54. Celi, P. (2018). Safety evaluation of dietarylevels of 25-hydroxyvitamin D 3 in growing calves.Food and Chemical Toxicology. Vol. 111, pp. 641–649. DOI:10.1016/j.fct.2017.11.053.
  55. Mearns, R. (2008). Rickets in sheep flocks innorthern England. Veterinary Record. Vol. 162, no. 3,pp. 98–99. DOI:10.1136/vr.162.3.98.
  56. Hurst, E. A., Homer, N. Z., Mellanby, R. J.(2020). Vitamin D Metabolism and Profiling in Veterinary Species. Metabolites. Vol. 10, no. 9, 371 p.DOI:10.3390/metabo10090371.
  57. Bandarra, P. M. (2011). Nutritional fibrous osteodystrophy in goats. Pesquisa Veterinária Brasileira.Vol. 31, no. 10, pp. 875–878. DOI:10.1590/S0100-736X20110 01000007.
  58. Maslak, Y., Mitrofanov, O., Sobakar, A. Biochemical diagnostics of osteodystrophy of goats. Lucrări Științifice-Universitatea de Științe Agricole șiMedicină Veterinară, Seria Zootehnie. Vol. 69, pp. 48–51. Available at:uaiasi.ro/firaa/Pdf/ Pdf_Vol_69/Y_Maslak.pdf.
  59. Van Saun, R. J. (2004). Vitamin D-responsiverickets in neonatal lambs. The Canadian VeterinaryJournal, Vol. 45, no. 1, 841 p. PMID:15532884.
  60. Melnyk, A. Y. (2021). Metabolic disorders inpoultry. Scientific Messenger of LNU of VeterinaryMedicine and Biotechnologies. Veterinary Sciences,Vol. 23 (103), pp. 125–135. Available at:nvlvet.com.ua/index.php/journal/article/view/4209/4304.
  61. Zaki, M. S. Natural Cases of Rickets in Baraki Goat Kids. Life Science Journal, Vol. 9, no. 1, pp.184–188. Available at:lifescencsite.com/lsj/life0901/026_7566life0901_184_188.pdf.
  62. Sharma, D. K., Sonawane, G. G., Swarnkar, C. P. (2017). Clinico-hemato-biochemical study oftwo commercial feed supplements for amelioration ofrickets in growing male lambs. Comparative ClinicalPathology. Vol. 27, no. 1, pp. 231–238. DOI:10.1007/s00580-017-2582-4.
  63. Thompson, K. (2007). An outbreak of ricketsin Corriedale sheep: Evidence for a genetic aeti-ology.New Zealand Veterinary Journal, Vol. 55, no. 3, pp.137–142. DOI:10.1080/0048 0169.2007.36757.
  64. Braun, U. (2009). Osteoporosis in goatsassociated with phosphorus and calcium deficiency. Veterinary Record. Vol. 164, no. 7, pp. 211–213.DOI:10.1136/vr.164.7.211.
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Scientific Journal of Veterinary Medicine 2'2023