Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Phosphate homeostasis is mostly regulated through humoral factors exerting direct or indirect effects on transporter proteins located in the intestine and kidney. Fibroblast growth factor 23 (FGF-23) is a major phosphate-regulating molecule, which can affect both renal and intestinal phosphate uptake to influence overall mineral ion homeostasis. We have found that Fgf-23 gene knockout mice (Fgf-23-/-) develop hyperphosphatemia that consequently leads to abnormal bone mineralization, and severe soft tissue calcifications. On the contrary, FGF-23 transgenic mice develop hypophosphatemia and produce rickets-like features in the mutant bone. Further studies using our Fgf-23 -/- mice have identified an inverse correlation between Fgf-23, and vitamin D or NaPi2a; genomic elimination of either vitamin D or NaPi2a activities from Fgf-23-/- mice could reverse severe hyperphosphatemia to hypophosphatemia, and consequently could alter skeletal mineralization, suggesting that regulation of phosphate homeostasis in Fgf-23-/- mice is vitamin D- and NaPi2a-mediated process.

Original languageEnglish (US)
Title of host publicationSkeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling
Pages485-493
Number of pages9
Volume1116
DOIs
StatePublished - Nov 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1116
ISSN (Print)00778923
ISSN (Electronic)17496632

Fingerprint

Sodium-Phosphate Cotransporter Proteins
Hyperphosphatemia
Metabolism
Vitamin D
Phosphates
Hypophosphatemia
Homeostasis
Bone
Kidney
Physiologic Calcification
Rickets
Gene Knockout Techniques
Knockout Mice
Transgenic Mice
Intestines
Minerals
Genes
Ions
Tissue
Bone and Bones

Keywords

  • Bone
  • Fgf-23
  • Phosphate regulation
  • Vitamin D

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Sitara, D. (2007). Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice. In Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling (Vol. 1116, pp. 485-493). (Annals of the New York Academy of Sciences; Vol. 1116). https://doi.org/10.1196/annals.1402.021

Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice. / Sitara, Despina.

Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling. Vol. 1116 2007. p. 485-493 (Annals of the New York Academy of Sciences; Vol. 1116).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Sitara, D 2007, Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice. in Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling. vol. 1116, Annals of the New York Academy of Sciences, vol. 1116, pp. 485-493. https://doi.org/10.1196/annals.1402.021
Sitara D. Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice. In Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling. Vol. 1116. 2007. p. 485-493. (Annals of the New York Academy of Sciences). https://doi.org/10.1196/annals.1402.021
Sitara, Despina. / Correlation among hyperphosphatemia, type II sodium-phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice. Skeletal Biology and Medicine, Part A: Aspects of Bone Morphogenesis and Remodeling. Vol. 1116 2007. pp. 485-493 (Annals of the New York Academy of Sciences).
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AB - Phosphate homeostasis is mostly regulated through humoral factors exerting direct or indirect effects on transporter proteins located in the intestine and kidney. Fibroblast growth factor 23 (FGF-23) is a major phosphate-regulating molecule, which can affect both renal and intestinal phosphate uptake to influence overall mineral ion homeostasis. We have found that Fgf-23 gene knockout mice (Fgf-23-/-) develop hyperphosphatemia that consequently leads to abnormal bone mineralization, and severe soft tissue calcifications. On the contrary, FGF-23 transgenic mice develop hypophosphatemia and produce rickets-like features in the mutant bone. Further studies using our Fgf-23 -/- mice have identified an inverse correlation between Fgf-23, and vitamin D or NaPi2a; genomic elimination of either vitamin D or NaPi2a activities from Fgf-23-/- mice could reverse severe hyperphosphatemia to hypophosphatemia, and consequently could alter skeletal mineralization, suggesting that regulation of phosphate homeostasis in Fgf-23-/- mice is vitamin D- and NaPi2a-mediated process.

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