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Phosphate Buffer01:22

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Phosphate-dependent FGF23 secretion is modulated by PiT2/Slc20a2.

Nina Bon1, Giulia Frangi1, Sophie Sourice1

  • 1Inserm, UMR 1229, RMeS, Regenerative Medicine and Skeleton, Université de Nantes, ONIRIS, Nantes, F-44042, France; Université de Nantes, UFR Odontologie, Nantes, F-44042, France.

Molecular Metabolism
|March 20, 2018
PubMed
Summary

The study identifies sodium-dependent phosphate transporter 2 (PiT2) as crucial for regulating fibroblast growth factor 23 (Fgf23) secretion, particularly under high phosphate conditions. Targeting PiT2 may help manage hyperphosphatemia in diseases like chronic kidney disease.

Keywords:
BoneFGF23 secretionPhosphate sensingPiT1/Slc20a1PiT2/Slc20a2

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Area of Science:

  • Bone biology
  • Endocrinology
  • Mineral metabolism

Background:

  • Fibroblast growth factor 23 (Fgf23) is a bone-derived hormone regulating serum inorganic phosphate (Pi) levels.
  • Serum Pi levels influence Fgf23 secretion via incompletely understood feedback mechanisms.
  • Previous in vitro studies implicated PiT1 and PiT2 transporters in Pi-dependent signaling.

Purpose of the Study:

  • To investigate the role of PiT1 and PiT2 in mediating Pi-dependent Fgf23 secretion.
  • To elucidate the contribution of these transporters to the feedback loop regulating Fgf23.

Main Methods:

  • Utilized PiT2 knockout (KO) mice and DMP1Cre; PiT1lox/lox mice fed modified diets.
  • Assessed Fgf23 secretion and expression of Pi homeostasis genes in vivo and ex vivo.
  • Employed adenovirus-mediated gene deletion in isolated long bone shafts.

Main Results:

  • PiT2 KO mice showed dysregulated Fgf23 secretion in response to low-Pi diets.
  • PiT2 was essential for appropriate Pi-dependent Fgf23 secretion in isolated bone shafts.
  • PiT1 deletion in osteocytes was inefficient, and its role in Pi-dependent Fgf23 regulation appeared minimal.
  • PiT2 appears to function as an endocrine Pi sensor, influencing Fgf23 levels independently of dietary Pi.

Conclusions:

  • Identified PiT2 as a key mediator of Pi-dependent Fgf23 secretion, especially under high Pi conditions.
  • Suggests PiT2 as a potential therapeutic target for managing excess FGF23 in hyperphosphatemic conditions like chronic kidney disease.