Calcium and Phosphate Hormones: Vitamin D, Parathyroid Hormone, and Fibroblast Growth Factor 23

2020 ◽  
Vol 41 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Lisa Underland ◽  
Morri Markowitz ◽  
Robert Gensure
2014 ◽  
Vol 82 (2014) (11) ◽  
pp. 296-303 ◽  
Author(s):  
Anna J. Jovanovich ◽  
Michel Chonchol ◽  
Christopher B. Brady ◽  
James D. Kaufman ◽  
Jessica Kendrick ◽  
...  

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1472 ◽  
Author(s):  
María E. Rodríguez-Ortiz ◽  
Mariano Rodríguez

Maintaining mineral metabolism requires several organs and hormones. Fibroblast growth factor 23 (FGF23) is a phosphatonin produced by bone cells that reduces renal production of calcitriol – 1,25(OH)2D3 – and induces phosphaturia. The consequences of a reduction in 1,25(OH)2D3 involve changes in calcium homeostasis. There are several factors that regulate FGF23: phosphorus, vitamin D, and parathyroid hormone (PTH). More recently, several studies have demonstrated that calcium also modulates FGF23 production. In a situation of calcium deficiency, the presence of 1,25(OH)2D3 is necessary to optimize intestinal absorption of calcium, and FGF23 is decreased to avoid a reduction in 1,25(OH)2D3 levels.


2007 ◽  
Vol 195 (1) ◽  
pp. 125-131 ◽  
Author(s):  
Tijana Krajisnik ◽  
Peyman Björklund ◽  
Richard Marsell ◽  
Östen Ljunggren ◽  
Göran Åkerström ◽  
...  

Fibroblast growth factor-23 (FGF23) is a circulating factor that decreases serum levels of inorganic phosphate (Pi) as well as 1,25-dihydroxyvitamin D3. Recent studies also suggest a correlation between serum levels of FGF23 and parathyroid hormone (PTH) in patients with chronic kidney disease. It is, however, unknown whether FGF23 directly modulates PTH expression, or whether the correlation is secondary to abnormalities in Pi and vitamin D metabolism. The objective of the current study was therefore to elucidate possible direct effects of FGF23 on bovine parathyroid cells in vitro. Treatment of parathyroid cells with a stabilized form of recombinant FGF23 (FGF23(R176Q)) induced a rise in early response gene-1 mRNA transcripts, a marker of FGF23 signaling. FGF23(R176Q) potently and dose-dependently decreased the PTH mRNA level within 12 h. In agreement, FGF23(R176Q) also decreased PTH secretion into conditioned media. In contrast, FGF23(R176Q) dose-dependently increased 1α-hydroxylase expression within 3 h. FGF23 (R176Q) did not affect cell viability nor induce apoptosis, whereas a small but significant increase in cell proliferation was found. We conclude that FGF23 is a negative regulator of PTH mRNA expression and secretion in vitro. Our data suggest that FGF23 may be a physiologically relevant regulator of PTH. This defines a novel function of FGF23 in addition to the previously established roles in controlling vitamin D and Pi metabolism.


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