Fibroblast Growth Factor 23 Mediates the Phosphaturic Actions of Cadmium

DOI Web Site Web Site PubMed 43 References
  • KIDO Shinsuke
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • FUJIHARA Marina
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • NOMURA Kengo
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • SASAKI Shohei
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • SHIOZAKI Yuji
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • SEGAWA Hiroko
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • TATSUMI Sawako
    Department of Molecular Nutrition, the University of Tokushima Graduate School
  • MIYAMOTO Ken-ichi
    Department of Molecular Nutrition, the University of Tokushima Graduate School

Bibliographic Information

Other Title
  • カドミウム曝露によるリン代謝異常～FGF23産生亢進機序の検討～
  • カドミウム バクロ ニ ヨル リン タイシャ イジョウ : FGF23 サンセイ コウシン キジョ ノ ケントウ

Search this article

Description

Phosphaturia has been documented following cadmium (Cd) exposure in both humans and experimental animals. Fibroblast growth factor 23 (FGF23) serves as an essential phosphate homeostasis pathway in the bone-kidney axis. In the present study, we investigated the effects of Cd on phosphate (Pi) homeostasis in mice. Following Cd injection into C57BL/6J mice, plasma FGF23 concentration significantly increased. The urinary Pi excretion level was significantly higher in the Cd-injected C57BL/6J mice than in the control group. Plasma Pi concentration decreased only slightly in the Cd-injected mice compared with the control group. No changes were observed in the concentration of the plasma parathyroid hormone and 1,25-dihydroxy vitamin D3 in both groups of mice. We observed a decrease in phosphate transport activity and also a decrease in the expression level of renal phosphate transporter Npt2c, but not that of Npt2a. Furthermore, we examined the effect of Cd on Npt2c in Npt2a-knockout (KO) mice, which expresses Npt2c as a major NaPi cotransporter. Injecting Cd to Npt2aKO mice induced a significant increase in plasma FGF23 concentration and urinary Pi excretion level. Furthermore, we observed decreases in phosphate transport activity and renal Npt2c expression level in the Cd-injected Npt2a KO mice. The present study suggests that hypophosphatemia induced by Cd may be closely associated with FGF23.<br>

Journal

References(43)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top