Calcium, phosphorus, and bone metabolism in the fetus and newborn☆
Introduction
Neonatal mineral and skeletal homeostasis represents a state of transition between fetal physiology, in which the placenta dominates to deliver and remove minerals, and adult physiology, in which the calciotropic hormones coordinate mineral handling by the intestines, kidneys, and bone. In order to understand this transition, it is first necessary to review the regulation of fetal mineral homeostasis, and then discuss the progressive changes that are provoked at birth.
The reader is referred to the author's much more comprehensive and detailed review that contains more than 750 citations of the primary data described herein [1]. Allotted space permits this brief monograph to serve only as a synopsis of the longer article.
Section snippets
Fetal calcium, phosphorus, and bone metabolism
The endochondral skeleton begins forming in the embryo, but it is not until the third trimester that substantial bone is formed and mineralized. The average human fetus has 30 g of calcium by term, with 80% of that accreted during the third trimester. Although the kidneys and intestines control the delivery and excretion of minerals in the adult, they are relatively unimportant for the normal fetus. Instead, it is the placenta that actively transports minerals from the maternal circulation, and
Neonatal calcium, phosphorus, and bone metabolism
When the umbilical cord is cut and the first breath is taken, these events trigger a rapid change in how mineral metabolism is regulated. The placental infusion and excretion of minerals are abruptly lost, while breathing causes an obligatory increase in blood pH. These alterations provoke a fall in serum calcium and ionized calcium. The intestines become the main source of minerals, the kidneys begin to reabsorb minerals, and bone turnover becomes more important to maintain serum mineral
Conclusions
Fetuses require PTHrP and PTH for placental mineral transfer, serum mineral concentrations, endochondral bone development, and skeletal mineralization, whereas calcitriol, calcitonin, and FGF23 are not essential (Fig. 1). It is during the neonatal period that intestinal calcium absorption becomes dependent upon vitamin D/calcitriol, and fetal kidneys become responsive to FGF23 (Fig. 1). This explains why rickets develops postnatally with disorders of vitamin D or FGF23.
Conflict of interest statement
None.
References (2)
Bone development and mineral homeostasis in the fetus and neonate: roles of the calciotropic and phosphotropic hormones
Physiol Rev
(2014)Fetal control of calcium and phosphate homeostasis — lessons from mouse models
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Grant support: Canadian Institutes of Health Research (grant #133413, #126469 and #84253) and Research & Development Corporation of Newfoundand and Labrador (grant #5404.1145.102).