Publication: Oral phosphate supplementation corrects hypophosphatemia and normalizes plasma FGF23 and 25-hydroxyvitamin D3 levels in women with chronic metabolic acidosis
Issued Date
2010-03-05
Resource Type
ISSN
14393646
09477349
09477349
Other identifier(s)
2-s2.0-77649153956
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Experimental and Clinical Endocrinology and Diabetes. Vol.118, No.2 (2010), 105-112
Suggested Citation
S. Domrongkitchaiporn, S. Disthabanchong, R. Cheawchanthanakij, K. Niticharoenpong, W. Stitchantrakul, N. Charoenphandhu, N. Krishnamra Oral phosphate supplementation corrects hypophosphatemia and normalizes plasma FGF23 and 25-hydroxyvitamin D3 levels in women with chronic metabolic acidosis. Experimental and Clinical Endocrinology and Diabetes. Vol.118, No.2 (2010), 105-112. doi:10.1055/s-0029-1202791 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/28762
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Oral phosphate supplementation corrects hypophosphatemia and normalizes plasma FGF23 and 25-hydroxyvitamin D3 levels in women with chronic metabolic acidosis
Other Contributor(s)
Abstract
Background: Chronic metabolic acidosis (CMA) is known to induce renal phosphate wasting and hypophosphatemia by enhancing bone resorption and inhibiting renal phosphate reabsorption. However, nothing is known regarding changes in the plasma levels of phosphate-regulating hormones during CMA, especially in humans with normal kidney function. Methods: Fifteen healthy Thai female volunteers were given NH4Cl orally for 7 days to induce CMA with or without oral phosphate supplementation. Blood and 24-h urine specimens were collected prior to and after CMA induction. Plasma concentrations and fractional excretion of calcium and inorganic phosphate as well as plasma levels of fibroblast growth factor (FGF) 23, 25(OH)D3, 1,25(OH) 2D3 and intact parathyroid hormone (iPTH) were determined. Results: CMA led to hypophosphatemia and hypocalcemia with increases in the fractional excretion of calcium and phosphate. Plasma concentrations of FGF23, 25(OH)D3 and iPTH were decreased, whereas that of 1,25(OH) 2D3 was increased. After oral phosphate supplementation, CMA-induced changes in the concentrations of the studied ions, FGF23 and 25(OH)D3, but not those of 1,25(OH)2D3 and iPTH, were diminished. Conclusions: The CMA-induced hypophosphatemia was likely to initiate a negative feedback response, thereby leading to reduction in the plasma levels of hyperphosphaturic hormones, FGF23 and PTH. An increase in the plasma 1,25(OH)2D3 level, despite diminishing 25(OH)D 3 storage pool, may help enhance the intestinal phosphate absorption. Oral phosphate supplementation abolished the effects of CMA on FGF23 and 25(OH)D3 levels, suggesting that the plasma phosphate concentration is the primary regulator of the plasma levels of these hormones during CMA. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart - New York.