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Fosfat Metabolizması

Year 2019, Volume: 19 Issue: 3, 105 - 115, 01.10.2019
https://doi.org/10.5222/j.child.2019.43650

Abstract

Serum fosfatın fizyolojik aralıkta korunması birçok biyolojik işlem için kritiktir. Fosfat, kemiklerin, nükleik asitlerin, hücre zarlarının önemli bir bileşenidir ve hücresel enerji metabolizmasında, proteinlerin fosforilasyonuyla hücre içi sinyalizasyonda ve hemoglobinden oksijen salınmasında önemli bir rol oynar. Fosfat önemli bir idrar ve kan asidi baz tamponudur 1 . Serum fosfor seviyesi, bağırsak emilimi, hücre içi ve kemik depo havuzlarının değişimi ve renal tübüler yeniden emilim arasındaki karmaşık bir etkileşimle sağlanır. Böbrek, tübüler yeniden emilim ile fosfor homeostazının düzenlenmesinde önemli bir rol oynar. Tip IIa ve tip IIc Na taşıyıcıları, proksimal tübüler hücrelerin fırça sınır membranında ifade edilen önemli renal Na bağımlı inorganik fosfat taşıyıcılardır. Her ikisi de diyet ile inorganik fosfat alımı, D vitamini, fibroblast büyüme faktörü 23 FGF23 ve paratiroid hormonu PTH tarafından düzenlenir 2 .

References

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Phosphate Metabolism

Year 2019, Volume: 19 Issue: 3, 105 - 115, 01.10.2019
https://doi.org/10.5222/j.child.2019.43650

Abstract

Maintenance of serum phosphate in the physiological range is critical for many biological processes. Phosphate is an essential component of bones, nucleic acids, and cell membranes, and it plays a crucial role in cellular energy metabolism, intracellular signaling by phosphorylation of proteins, and release of oxygen from hemoglobin. Phosphate is an important urinary and blood acid base buffer 1 . The serum phosphorus level is maintained through a complex interplay between intestinal absorption, exchange intracellular and bone storage pools, and renal tubular reabsorption. The kidney plays a major role in regulation of phosphorus homeostasis by renal tubular reabsorption. Type IIa and type IIc Na transporters are important renal Na dependent inorganic phosphate transporters, which are expressed in the brush border membrane of proximal tubular cells. Both are regulated by dietary inorganic phosphate intake, vitamin D, fibroblast growth factor 23 FGF23 and parathyroid hormone 2 .

References

  • 1. Gattineni J, Baum M. Genetic disorders of phosphate regulation. Pediatric Nephrology (Berlin, Germany). 2012;27(9):1477-87.
  • 2. Choi NW. Kidney and phosphate metabolism. Electrolyte & Blood Pressure, 2008;6(2):77-85.
  • 3. Amanzadeh J, Reilly RF, Jr. Hypophosphatemia: an evidence-based approach to its clinical consequences and management. Nature Clinical Practice Nephrology. 2006;2(3):136-48.
  • 4. Alizadeh Naderi AS, Reilly RF. Hereditary disorders of renal phosphate wasting. Nature reviews Nephrology. 2010;6(11):657-65.
  • 5. Farrow EG, White KE. Recent advances in renal phosphate handling. Nature reviews Nephrology. 2010;6(4):207-17.
  • 6. Berndt TJ, Schiavi S, Kumar R. “Phosphatonins” and the regulation of phosphorus homeostasis. American journal of physiology. Renal physiology. 2005;289(6):F1170- 82.
  • 7. Bergwitz C, Juppner H. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annual review of medicine. 2010;61:91-104.
  • 8. Alon US. Clinical practice. Fibroblast growth factor (FGF)23: a new hormone. European journal of pediatrics. 2011;170(5):545-54.
  • 9. Jubiz W, Canterbury JM, Reiss E, Tyler FH. Circadian rhythm in serum parathyroid hormone concentration in human subjects: correlation with serum calcium, phosphate, albumin, and growth hormone levels. The Journal of clinical investigation. 1972;51(8):2040-6.
  • 10. Lichtman MA, Miller DR, Cohen J, Waterhouse C. Reduced red cell glycolysis, 2, 3-diphosphoglycerate and adenosine triphosphate concentration, and increased hemoglobin-oxygen affinity caused by hypophosphatemia. Annals of internal medicine. 1971;74(4):562-8.
  • 11. Schubert L, DeLuca HF. Hypophosphatemia is responsible for skeletal muscle weakness of vitamin D deficiency. Archives of biochemistry and biophysics. 2010;500(2):157-61.
  • 12. Knochel JP. The pathophysiology and clinical characteristics of severe hypophosphatemia. Archives of Internal Medicine. 1977;137(2):203-20.
  • 13. Knochel JP. Hypophosphatemia and rhabdomyolysis. The American Journal of Medicine. 1992;92(5):455-7.
  • 14. Newman JH, Neff TA, Ziporin P. Acute respiratory failure associated with hypophosphatemia. The New England Journal of Medicine. 1977;296(19):1101-3.
  • 15. O’Connor LR, Wheeler WS, Bethune JE. Effect of hypophosphatemia on myocardial performance in man. The New England journal of medicine. 1977;297(17):901-3.
  • 16. Kalantar-Zadeh K, Gutekunst L, Mehrotra R, Kovesdy CP, Bross R, Shinaberger CS, et al. Understanding sources of dietary phosphorus in the treatment of patients with chronic kidney disease. Clinical Journal of the American Society of Nephrology : CJASN. 2010;5(3):519- 30.
  • 17. Ramirez JA, Emmett M, White MG, Fathi N, Santa Ana CA, Morawski SG, et al. The absorption of dietary phosphorus and calcium in hemodialysis patients. Kidney international. 1986;30(5):753-9.
  • 18. Gupta RK, Gangoliya SS, Singh NK. Reduction of phytic acid and enhancement of bioavailable micronutrients in food grains. Journal of food science and technology. 2015;52(2):676-84.
  • 19. Moe SM, Zidehsarai MP, Chambers MA, Jackman LA, Radcliffe JS, Trevino LL, et al. Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease. Clinical journal of the American Society of Nephrology : CJASN. 2011;6(2):257-64.
  • 20. McCutcheon J, Campbell K, Ferguson M, Day S, Rossi M. Prevalence of Phosphorus-Based Additives in the Australian Food Supply: A Challenge for Dietary Education? Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation. 2015;25(5):440-4.
  • 21. Uribarri J, Calvo MS. Hidden sources of phosphorus in the typical American diet: does it matter in nephrology? Seminars in dialysis. 2003;16(3):186-8.
  • 22. Leon JB, Sullivan CM, Sehgal AR. The prevalence of phosphorus-containing food additives in top-selling foods in grocery stores. Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation. 2013;23(4):265-70.e2.
  • 23. Wesseling-Perry K. FGF-23 in bone biology. Pediatric nephrology (Berlin, Germany). 2010;25(4):603-8.
  • 24. Xu H, Collins JF, Bai L, Kiela PR, Ghishan FK. Regulation of the human sodium-phosphate cotransporter NaP(i)- IIb gene promoter by epidermal growth factor. American Journal of Physiology Cell physiology. 2001;280(3):C628-36.
  • 25. Arima K, Hines ER, Kiela PR, Drees JB, Collins JF, Ghishan FK. Glucocorticoid regulation and glycosylation of mouse intestinal type IIb Na-P(i) cotransporter during ontogeny. American journal of physiology Gastrointestinal and liver physiology. 2002;283(2):G426- 34.
  • 26. Xu H, Uno JK, Inouye M, Xu L, Drees JB, Collins JF, et al. Regulation of intestinal NaPi-IIb cotransporter gene expression by estrogen. American journal of physiology Gastrointestinal and liver physiology. 2003;285(6):G1317-24.
  • 27. Stauber A, Radanovic T, Stange G, Murer H, Wagner CA, Biber J. Regulation of intestinal phosphate transport. II. Metabolic acidosis stimulates Na(+)-dependent phosphate absorption and expression of the Na(+)-P(i) cotransporter NaPi-IIb in small intestine. American journal of physiology Gastrointestinal and liver physiology. 2005;288(3):G501-6.
  • 28. Danisi G, Bonjour JP, Straub RW. Regulation of Na-dependent phosphate influx across the mucosal border of duodenum by 1,25-dihydroxycholecalciferol. Pflugers Archiv: European journal of physiology. 1980;388(3):227-32.
  • 29. Hattenhauer O, Traebert M, Murer H, Biber J. Regulation of small intestinal Na-P(i) type IIb cotransporter by dietary phosphate intake. The American journal of physiology. 1999;277(4):G756-62.
  • 30. Hilfiker H, Hattenhauer O, Traebert M, Forster I, Murer H, Biber J. Characterization of a murine type II sodiumphosphate cotransporter expressed in mammalian small intestine. Proceedings of the National Academy of Sciences of the United States of America. 1998;95(24):14564-9.
  • 31. Virkki LV, Biber J, Murer H, Forster IC. Phosphate transporters: a tale of two solute carrier families. American journal of physiology Renal physiology. 2007;293(3):F643-54.
  • 32. Villa-Bellosta R, Ravera S, Sorribas V, Stange G, Levi M, Murer H, et al. The Na+-Pi cotransporter PiT-2 (SLC20A2) is expressed in the apical membrane of rat renal proximal tubules and regulated by dietary Pi. American journal of physiology Renal physiology. 2009;296(4):F691-9.
  • 33. Villa-Bellosta R, Sorribas V. Compensatory regulation of the sodium/phosphate cotransporters NaPi-IIc (SCL34A3) and Pit-2 (SLC20A2) during Pi deprivation and acidosis. Pflugers Archiv : European journal of physiology. 2010;459(3):499-508.
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Primary Language Turkish
Journal Section Collection
Authors

Hasan Önal This is me

Publication Date October 1, 2019
Published in Issue Year 2019 Volume: 19 Issue: 3

Cite

APA Önal, H. (2019). Fosfat Metabolizması. Çocuk Dergisi, 19(3), 105-115. https://doi.org/10.5222/j.child.2019.43650
AMA Önal H. Fosfat Metabolizması. Çocuk Dergisi. October 2019;19(3):105-115. doi:10.5222/j.child.2019.43650
Chicago Önal, Hasan. “Fosfat Metabolizması”. Çocuk Dergisi 19, no. 3 (October 2019): 105-15. https://doi.org/10.5222/j.child.2019.43650.
EndNote Önal H (October 1, 2019) Fosfat Metabolizması. Çocuk Dergisi 19 3 105–115.
IEEE H. Önal, “Fosfat Metabolizması”, Çocuk Dergisi, vol. 19, no. 3, pp. 105–115, 2019, doi: 10.5222/j.child.2019.43650.
ISNAD Önal, Hasan. “Fosfat Metabolizması”. Çocuk Dergisi 19/3 (October 2019), 105-115. https://doi.org/10.5222/j.child.2019.43650.
JAMA Önal H. Fosfat Metabolizması. Çocuk Dergisi. 2019;19:105–115.
MLA Önal, Hasan. “Fosfat Metabolizması”. Çocuk Dergisi, vol. 19, no. 3, 2019, pp. 105-1, doi:10.5222/j.child.2019.43650.
Vancouver Önal H. Fosfat Metabolizması. Çocuk Dergisi. 2019;19(3):105-1.