Forskning
Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Fibroblast Growth Factor (FGF) 23 Regulates the Plasma Levels of Parathyroid Hormone In Vivo Through the FGF Receptor in Normocalcemia, But Not in Hypocalcemia

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Multiple Fractures and Impaired Bone Fracture Healing in a Patient with Pycnodysostosis and Hypophosphatasia

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Chronic Non-bacterial Osteomyelitis: A Review

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

  3. Bone mass development in childhood and its association with physical activity and vitamin D levels. The CHAMPS-Study DK

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Circadian rhythm of activin A and related parameters of mineral metabolism in normal and uremic rats

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Challenges and opportunities for nephrology in Western Europe

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Nye hormoner relateret til calcium- og fosfathomøostasen ved nyresygdom

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Effect of inhibition of CBP-coactivated β-catenin-mediated Wnt signalling in uremic rats with vascular calcifications

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

The calcium and phosphate homeostasis is regulated by a complex interplay between parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and calcitriol. Experimental studies have demonstrated an inhibitory effect of FG23 on PTH production and secretion; the physiological role of this regulation is however not well understood. Surprisingly, in uremia, concomitantly elevated FGF23 and PTH levels are observed. The parathyroid gland rapidly loses its responsiveness to extracellular calcium in vitro and a functional parathyroid cell line has currently not been established. Therefore, the aim of the present investigation was to study the impact of FGF23 on the Ca2+/PTH relationship in vivo under conditions of normocalcemia and hypocalcemia. Wistar rats were allocated to treatment with intravenous recombinant FGF23 and inhibition of the FGF receptor in the setting of normocalcemia and acute hypocalcemia. We demonstrated that FGF23 rapidly inhibited PTH secretion and that this effect was completely blocked by inhibition of the FGF receptor. Furthermore, inhibition of the FGF receptor by itself significantly increased PTH levels, indicating that FGF23 has a suppressive tonus on the parathyroid gland's PTH secretion. In acute hypocalcemia, there was no effect of either recombinant FGF23 or FGF receptor inhibition on the physiological response to the low ionized calcium levels. In conclusion, FGF23 has an inhibitory tonus on PTH secretion in normocalcemia and signals through the FGF receptor. In acute hypocalcemia, when increased PTH secretion is needed to restore the calcium homeostasis, this inhibitory effect of FGF23 is abolished.

OriginalsprogEngelsk
TidsskriftCalcified Tissue International
Vol/bind102
Udgave nummer1
Sider (fra-til)85-92
Antal sider8
ISSN0171-967X
DOI
StatusUdgivet - 2018

ID: 52424539