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Udgivet

Circulating FGF23 levels in response to acute changes in plasma Ca(2+)

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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The regulation of fibroblast growth factor 23 (FGF23) synthesis and secretion is still incompletely understood. FGF23 is an important regulator of renal phosphate excretion and has regulatory effects on the calciotropic hormones calcitriol and parathyroid hormone (PTH). Calcium (Ca) and phosphate homeostasis are closely interrelated, and it is therefore likely that Ca is involved in FGF23 regulation. It has recently been reported that dietary Ca influenced FGF23 levels, with high Ca increasing FGF23. The mechanism remains to be clarified. It remains unknown whether acute changes in plasma Ca influence FGF23 levels and whether a close relationship, similar that known for Ca and PTH, exists between Ca and FGF23. Thus, the aim of the present study was to examine whether acute hypercalcemia and hypocalcemia regulate FGF23 levels in the rat. Acute hypercalcemia was induced by an intravenous Ca infusion and hypocalcemia by infusion of ethylene glycol tetraacetic acid (EGTA) in normal and acutely parathyroidectomized rats. Intact plasma FGF23 and intact plasma PTH and plasma Ca(2+) and phosphate were measured. Acute hypercalcemia and hypocalcemia resulted as expected in adequate PTH secretory responses. Plasma FGF23 levels remained stable at all plasma Ca(2+) levels; acute parathyroidectomy did not affect FGF23 secretion. In conclusion, Ca is not a regulator of acute changes in FGF23 secretion
OriginalsprogEngelsk
TidsskriftCalcified Tissue International
Vol/bind95
Udgave nummer1
Sider (fra-til)46-53
Antal sider8
ISSN0171-967X
DOI
StatusUdgivet - jul. 2014

ID: 44823392