Abstract
Fetal calcium and bone metabolism differs from that of the adult, having been uniquely adapted to meet the specific needs of this developmental period. If these regulatory processes in the fetus were more fully elucidated and understood, the insight gained might lead to the development of novel therapies for osteoporosis and other metabolic bone diseases. We have explored the regulation of normal fetal calcium physiology through the use of gene targeting models. These techniques permit the study of fetal models that cannot be created by surgical or pharmacological techniques, such as fetal mice whose parathyroids produce parathyroid hormone (PTH) but not PTH-related protein (PTHrP), and vice versa. This article briefly reviews what we have learned from these studies, in the context of what is already known about fetal calcium homeostasis. Drug Dev. Res. 49:167–173, 2000. © 2000 Wiley-Liss, Inc.
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