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- W1636707060 endingPage "302" @default.
- W1636707060 startingPage "271" @default.
- W1636707060 abstract "This chapter reviews fetal mineral homeostasis as extrapolated from human and animal data, including older studies involving surgically manipulated fetuses and more recent studies of genetically engineered mice that lack calcitropic hormones or receptors. It is evident that fetal calcium and bone metabolism has been uniquely adapted to meet the specific needs of this developmental period, including the requirement to provide sufficient calcium to fully mineralize the skeleton and the requirement to maintain an extracellular level of calcium (and other minerals) that is physiologically appropriate for fetal tissues (for cell membrane stability and blood coagulation). A human fetus typically accumulates 21 g of calcium by term and 80% of this calcium is accumulated in the third trimester, necessitating an average daily transfer of 200–300mg calcium. The studies reviewed in the chapter demonstrate that the fetal-placental unit functions relatively independently of the mother, such that it is capable of mineralizing the fetal skeleton and maintaining normal blood calcium, even in the presence of significant maternal hypocalcemia and vitamin D deficiency. PTH-related protein (PTHrP) is a major regulator of placental calcium transport, whereas PTHrP and parathyroid hormone (PTH) act in concert to regulate the blood calcium and control skeletal mineralization." @default.
- W1636707060 created "2016-06-24" @default.
- W1636707060 creator A5012218281 @default.
- W1636707060 date "2003-01-01" @default.
- W1636707060 modified "2023-10-10" @default.
- W1636707060 title "Fetal Mineral Homeostasis" @default.
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