The following fluorinated phosphate esters haye been prepared: tris-(1 : I-di-H-heptafluorobutyl) phosphatc; tris-(u-trifluoromethylphcnyl) phosphate; bis-(nz-trifluoromethylphenyl) (1 : 1 -di-H-trifluoroethyl) phosphate; 2 : 2 : 3 : 3-tetrafluorotetramethylene-1 : 4-di-(bis-2 : 2 : 2-trifluoroethyl phosphate). In addition, the new compounds (1 : 1 -di-H-trifluoroethyl) phosphorodichloridate and bis-( 1 : I-di-H-trifluoroethyl) phosphorochloridntc were prepared.

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Vitamin D receptor (VDR) null fetuses have normal serum minerals, parathyroid hormone (PTH), skeletal morphology, and mineralization but increased serum calcitriol, placental calcium transport, and placental expression of Pthrp, Trpv6, and (as reported in this study) Pdia3. We examined Cyp27b1 null fetal mice, which do not make calcitriol, to determine if loss of calcitriol has the same consequences as loss of VDR. Cyp27b1 null and wild‐type (WT) females were mated to Cyp27b1+/‐ males, which generated Cyp27b1 null and Cyp27b1+/‐ fetuses from Cyp27b1 null mothers, and Cyp27b1+/‐ and WT fetuses from WT mothers. Cyp27b1 null fetuses had undetectable calcitriol but normal serum calcium and phosphorus, PTH, fibroblast growth factor 23 (FGF23), skeletal mineral content, tibial lengths and morphology, placental calcium transport, and expression of Trpv6 and Pthrp; conversely, placental Pdia3 was downregulated. However, although Cyp27b1+/‐ and null fetuses of Cyp27b1 null mothers were indistinguishable, they had higher serum and amniotic fluid calcium, lower amniotic fluid phosphorus, lower FGF23, and higher 25‐hydroxyvitamin D and 24,25‐dihydroxyvitamin D than in WT and Cyp27b1+/‐ fetuses of WT mothers. In summary, loss of fetal calcitriol did not alter mineral or bone homeostasis, but Cyp27b1 null mothers altered mineral homeostasis in their fetuses independent of fetal genotype. Cyp27b1 null fetuses differ from Vdr null fetuses, possibly through high levels of calcitriol acting on Pdia3 in Vdr nulls to upregulate placental calcium transport and expression of Trpv6 and Pthrp. In conclusion, maternal calcitriol influences fetal mineral metabolism, whereas loss of fetal calcitriol does not. © 2018 American Society for Bone and Mineral Research.

Fibroblast growth factor 23 (FGF23) appears to play no role until after birth, given unaltered phosphate and bone metabolism in Fgf23 and Klotho null fetuses. However, in those studies maternal serum phosphorus was normal. We studied whether maternal phosphate loading alters fetal serum phosphorus and invokes a fetal FGF23 or PTH response. C57BL/6 (WT) female mice received low (0.3%), normal (0.7%) or high (1.65%) phosphate diets beginning one week prior to mating to WT males. Fgf23  +/- female mice received the normal or high phosphate diets one week before mating to Fgf23  +/- males. One day before expected birth, we harvested maternal and fetal blood, intact fetuses, placentas, and fetal kidneys. Increasing phosphate intake in WT resulted in progressively higher maternal serum phosphorus and FGF23 during pregnancy, while PTH remained undetectable. Fetal serum phosphorus was independent of the maternal phosphorus, PTH remained low, but FGF23 showed a small non-significant increase with high maternal serum phosphorus. There were no differences in fetal ash weight and mineral content, or placental gene expression. High phosphate intake in Fgf23  +/- mice also increased maternal serum phosphorus and FGF23 but there was no change in PTH. WT fetuses remained unaffected by maternal high phosphate intake, while Fgf23 null fetuses became hyperphosphatemic but had no change in PTH, skeletal ash weight or mineral content. In conclusion, fetal phosphate metabolism is generally regulated independently of maternal serum phosphorus, and fetal FGF23 or PTH. However, maternal phosphate loading reveals that fetal FGF23 can defend against the development of fetal hyperphosphatemia.

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