The demands of fetal growth lead to an adaptation of maternal homeostasis 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)2D which shows quantitative rather than qualitative changes from the non-pregnant state. In contrast the maintenance of fetal mineral homeostasis largely depends on PTHrP which regulates active placental calcium transfer and the calcium fluxes across the 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 play a role in calcium homeostasis by acting through the PTH receptor.