Current concepts in perinatal mineral metabolism

Abstract

The serum levels of calcium (Ca) and phosphate are maintained higher in the fetus than in the pregnant mother, especially in late gestation, to meet the demands of fetal bone development. In order to maintain this fetal stage-specific mineral homeostasis, the placenta plays a critical role through active transcellular mineral transport. Although the molecular mechanism of transplacental Ca transport has been well studied, little is known about the transport mechanism of phosphate and magnesium. Maternal mineral homeostasis is also altered during pregnancy to supply minerals to the fetus. In the lactating mother, osteocytic osteolysis is suggested to be involved in the supply of minerals to the baby. The levels of some calcitropic and phosphotropic (Ca- and phosphate-regulating, respectively) hormones in the fetus are also different from those in the adult. The PTH level in the fetus is lower than that in the mother and nonpregnant adult. It is suggested, however, that low fetal PTH plays an important role in fetal mineral metabolism. The concentration of PTHrP in the fetus is much higher than that of PTH and plays a critical role in perinatal Ca homeostasis. Uncovering the molecular mechanisms for fetal stage-specific mineral metabolism will lead to better management of perinatal patients with mineral abnormalities.

Keywords: calcium; fetus; phosphate; placenta.

Fig. 1.

The feto-maternal interface of the placenta expressed Npt2b/NPT2B in both mice and humans. Immunohistochemical staining using antibodies against the type IIb Na+/Pi cotransporter (Npt2b/NPT2B) in ICR mouse placentas at E18.5 and normal human placentas at 38 wk of gestation. The signals for these proteins were detected in the syncytiotrophoblasts of mouse and human placentas. Sections were counterstained with hematoxylin. Scale bars, 50 μm.