Purpose of review The demand for calcium for milk production to supply the rapidly mineralizing neonatal skeleton places significant stress on maternal calcium homeostasis. The rapid and transient loss of maternal bone mineral density that accompanies lactation is an important mechanism to meet this demand. Previous evidence has suggested that low estrogen levels and high parathyroid hormone-related protein levels may mediate the mobilization of maternal skeletal calcium during lactation. This review describes recent work solidifying the role of parathyroid hormone-related protein produced by the mammary gland in maternal bone metabolism during lactation. The function of the calcium-sensing receptor on mammary cells during lactation is also discussed. Recent findings Estrogen treatment of lactating mice partially inhibited bone loss, indicating that factors other than estrogen deficiency are also involved. Selective deletion of the parathyroid hormone-related protein gene from the lactating mammary gland resulted in decreased circulating levels of parathyroid hormone-related protein and preservation of maternal bone mineral density. Finally, the calcium-sensing receptor is expressed on mammary epithelial cells and regulates their production of parathyroid hormone-related protein and the transport of calcium into milk. Summary A feedback mechanism is proposed in which the mammary gland performs the function of the parathyroid gland during lactation but uses parathyroid hormone-related protein rather than parathyroid hormone.
No takes yet. Share an insight, caveat, or question.
Joshua VanHouten (2005) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: