Searchable abstracts of presentations at key conferences on calcified tissues
Bone Abstracts (2014) 3 OC1.2 | DOI: 10.1530/boneabs.3.OC1.2

ECTS2014 Oral Communications Phosphate metabolism, fracture repair and osteoarthritis (6 abstracts)

Study of Hyp or Phex null male fetuses reveals that eightfold increased FGF23 does not alter fetal–placental phosphorus homeostasis or prenatal bone formation and mineralization

Yue Ma , Beth J. Kirby & Christopher S. Kovacs

Memorial University of Newfoundland, St. John’s, Newfoundland, Canada.

Fibroblast growth factor-23 (FGF23) controls serum phosphorus by acting on the kidneys to excrete phosphorus and reduce calcitriol. These actions are well established in adults and children, but whether FGF23 regulates fetal phosphorus metabolism is unknown. We used X-linked Hyp or Phex null male fetuses to study the effect of excess FGF23 on fetal phosphorus metabolism. Phex+/− females and WT males were mated to generate WT, Phex+/− female, and Phex null male fetuses. Reverse matings of WT female to Phex null males were also done. All studies were approved by the local ethics committee.

Phex+/− mothers had low serum phosphorus compared to WT mothers, but maternal hypophosphatemia did not affect fetal serum phosphorus levels. Phex+/− female and Phex null male fetuses had 7.8-fold higher serum FGF23 levels than WT littermates. Increased FGF23 did not affect fetal serum calcium and phosphorus, urine (amniotic fluid) calcium and phosphorus, parathyroid hormone, skeletal morphology or limb lengths, tibial growth plate morphology, skeletal ash weight, and skeletal calcium and phosphorus. Serum calcitriol was reduced in Phex null male fetuses (WT 52.0±5.8, Phex null 34.7±2.6 pmol/l, P<0.013). We administered 32P/51Cr-EDTA by intracardiac injection to pregnant mothers and found no difference among genotypes in placental transport of 32P after 5 min. WT placentas and fetal kidneys abundantly expressed FGF23 target genes, including Cyp27b1, Cyp24a1, Klotho, NaPi2a, NaPi2b, NaPi2c, and FGF receptors 1–4. Of these, Cyp24a1 was significantly increased in Phex null placentas and fetal kidneys, while Klotho was significantly reduced in Phex null kidneys. However, these changes in gene expression did not disturb fetal phosphorus parameters.

In conclusion, FGF23 is not an important regulator of fetal phosphorous metabolism. The active delivery of phosphorus across the placenta does not require FGF23 and overrides any effect that excess FGF23 might otherwise have on phosphate handling by fetal kidneys.

Volume 3

European Calcified Tissue Society Congress 2014

Prague, Czech Republic
17 May 2014 - 20 May 2014

European Calcified Tissue Society 

Browse other volumes

Article tools

My recent searches

No recent searches.