The skeleton: Endocrine regulator of phosphate homeostasis

@article{Doyle2008TheSE,
  title={The skeleton: Endocrine regulator of phosphate homeostasis},
  author={M{\'a}ire E. Doyle and Suzanne Jan de Beur},
  journal={Current Osteoporosis Reports},
  year={2008},
  volume={6},
  pages={134-141}
}
Phosphorus is an essential element in skeletal development, bone mineralization, membrane composition, nucleotide structure, and cellular signaling. Phosphate, the principal form in which phosphorus is found in the body, is regulated by the complex interplay of the hormones parathyroid hormone (PTH), calcitriol (1,25[OH]2 vitamin D3), and fibroblast growth factor 23 (FGF23). These collectively govern bone mineralization, absorption of phosphorus by the intestine, and renal tubular reabsorption… Expand
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References

SHOWING 1-10 OF 50 REFERENCES
Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism.
TLDR
Evidence is presented that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF 23-null mice, indicating that F GF23 is essential for normal phosphate and vitamin D metabolism. Expand
The parathyroid is a target organ for FGF23 in rats.
TLDR
It is shown that FGF23 acts directly on the parathyroid through the MAPK pathway to decrease serum PTH, which adds a new dimension to the understanding of mineral homeostasis. Expand
Bone as a source of FGF23: regulation by phosphate?
TLDR
The results indicate that FGF23 mRNA expression in bone cells is regulated by extracellular phosphate and by mineralization, and support proposals that bone may be a source of circulating FGF 23 and suggest that F GF23 expression by bone is regulated. Expand
Vitamin D receptor-independent FGF23 actions in regulating phosphate and vitamin D metabolism.
TLDR
FGF23 works, at at least in part, in a VDR-independent manner, and FGF23 production is also regulated by multiple mechanisms involving V DR-independent pathways. Expand
Mineralized tissue cells are a principal source of FGF23.
TLDR
The data suggest that FGF23 expression in bone is closely correlated with bone formation in vitro and vivo, and points towards an important role(s) for FGF 23 in young adult but not fetal mineralized tissues as a systemic factor for Pi homeostasis. Expand
Fibroblast growth factor 23 impairs phosphorus and vitamin D metabolism in vivo and suppresses 25-hydroxyvitamin D-1alpha-hydroxylase expression in vitro.
TLDR
Novel findings provide evidence that FGF-23 directly regulates renal 1alpha-hydroxylase gene expression via activation of the ERK1/2 signaling pathway. Expand
Circulating FGF-23 Is Regulated by 1α,25-Dihydroxyvitamin D3 and Phosphorus in Vivo*
TLDR
There was a feedback loop existing among serum phosphorus, 1α,25(OH)2D3, and FGF-23, in which the novel phosphate-regulating bone-kidney axis integrated with the parathyroid hormone-vitamin D3 axis in regulating phosphate homeostasis. Expand
The roles of specific genes implicated as circulating factors involved in normal and disordered phosphate homeostasis: frizzled related protein-4, matrix extracellular phosphoglycoprotein, and fibroblast growth factor 23.
TLDR
This review will focus upon recently discovered factors that are overexpressed in tumors associated with tumor-induced osteomalacia and have reported activity consistent with effecting Pi balance in vivo. Expand
FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate.
TLDR
The results suggest that FGF-23 is involved in the pathogenesis of these three hypophosphatemic disorders and directly link PHEX and F GF-23 within the same biochemical pathway. Expand
Inhibition of Intestinal Sodium‐dependent Inorganic Phosphate Transport by Fibroblast Growth Factor 23
  • K. Miyamoto, Mikiko Ito, M. Kuwahata, S. Kato, H. Segawa
  • Medicine
  • Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy
  • 2005
TLDR
The present study suggests that FGF23(R179Q) reduces intestinal sodium‐dependent Pi transport activity and type IIb NaPi protein levels by a mechanism that is dependent on VDR. Expand
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