Parathyroid hormone‐related peptide increases urinary phosphate excretion in fetal lambs

Davicco, MJ; Coxam,; Lefaivre, J.; Barlet, J.P.

doi:10.1113/expphysiol.1992.sp003598

Cited by 15 publications

(4 citation statements)

References 20 publications

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“…Pharmacological administration of NH 2 -terminal fragments of PTH or PTHrP increased serum calcium and reduced renal calcium excretion, but did not alter serum phosphorus or urine phosphorus excretion (142,398). These results may indicate that thyroparathyroidectomy causes hypocalcemia in part through loss of the effects of parathyroid-derived PTH and PTHrP on the renal tubules.…”

Section: Animal Datamentioning

confidence: 53%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

208

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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Section: Animal Datamentioning

confidence: 53%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

208

188

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“…A suckling-induced phosphaturia attributable to PTHrP has also been demonstrated in rats, goats, cows, and sheep (56,226,907,1003).…”

Section: Animal Datamentioning

confidence: 95%

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Kovacs

2016

Physiological Reviews

372

524

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During pregnancy and lactation, female physiology adapts to meet the added nutritional demands of fetuses and neonates. An average full-term fetus contains ϳ30 g calcium, 20 g phosphorus, and 0.8 g magnesium. About 80% of mineral is accreted during the third trimester; calcium transfers at 300-350 mg/day during the final 6 wk. The neonate requires 200 mg calcium daily from milk during the first 6 mo, and 120 mg calcium from milk during the second 6 mo (additional calcium comes from solid foods). Calcium transfers can be more than double and triple these values, respectively, in women who nurse twins and triplets. About 25% of dietary calcium is normally absorbed in healthy adults. Average maternal calcium intakes in American and Canadian women are insufficient to meet the fetal and neonatal calcium requirements if normal efficiency of intestinal calcium absorption is relied upon. However, several adaptations are invoked to meet the fetal and neonatal demands for mineral without requiring increased intakes by the mother. During pregnancy the efficiency of intestinal calcium absorption doubles, whereas during lactation the maternal skeleton is resorbed to provide calcium for milk. This review addresses our current knowledge regarding maternal adaptations in mineral and skeletal homeostasis that occur during pregnancy, lactation, and post-weaning recovery. Also considered are the impacts that these adaptations have on biochemical and hormonal parameters of mineral homeostasis, the consequences for long-term skeletal health, and the presentation and management of disorders of mineral and bone metabolism.

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“…Other renal effects of PTH and PTHrP common to fetus and adult include an increase in urinary pH and a decrease in free water clearance. Although large doses of PTHrP (3 nmol bolus + 3 nmol over 30 minutes) also induce phosphaturia (Davicco et al, 1992), it is uncertain whether this is a specific effect or one due to an 0 1996 Blackwell Science Ltd, Clinical Endocrinology, 45, 1-6 Calcium homeostasis in p r e g n a n c y 5 increase in GFR. Smaller doses (1 nmol/2 h) did not change G F R or induce phosphaturia although serum calcium rose (MacIsaac et al, 1993).…”

Section: Renat Function and Maternallfetal Minerat Homeostasismentioning

confidence: 99%

Calcium homeostasis in pregnancy

Hosking¹

1996

Clin Endocrinol

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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.

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Parathyroid hormone‐related peptide increases urinary phosphate excretion in fetal lambs

Abstract: SUMMARYThe effect of synthetic human parathyroid hormone-related

Cited by 15 publications

References 20 publications

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Calcium homeostasis in pregnancy

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