The demands of fetal growth lead to an adaptation of maternal homeosta
sis in order to provide the required calcium from enhanced intestinal
absorption rather than from mobilization of maternal skeletal reserves
. In large part this adaptive process depends on the interrelationship
between PTH and 1,25(OH)(2)D which shows quantitative rather than qua
litative changes from the non-pregnant state. In contrast the maintena
nce of fetal mineral homeostasis largely depends on PTHrP which regula
tes active placental calcium transfer and the calcium fluxes across th
e kidney and bone. The major source of PTHrP is the fetal parathyroid
gland although some is provided by the placenta. It may be this latter
component which passes into the maternal circulation where it may pla
y a role in calcium homeostasis by acting through the PTH receptor.