Perinatal Primate Parathyroid Hormone Metabolism

Fleischman, Alan R.; Lerman, Samuel; Oakes, Gary K.; Epstein, Michael F.; Chez, Ronald A.; Mintz, Daniel H.

doi:10.1159/000240757

Cited by 17 publications

(3 citation statements)

References 10 publications

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“…Typically the fetal serum calcium is 0.30 -0.50 mM or higher than the maternal level in rhesus monkeys (189,524), lambs (148,201,435,505), calves (201,715), rodents (201,338,340,342,346,347,623), pigs (98,101,353), and foals (201). The ionized calcium is also increased 0.25-0.50 mM above the maternal value in fetal rodents (148,340,422), confirming that true hypercalcemia is present relative to maternal and normal adult values.…”

Section: Animal Datamentioning

confidence: 87%

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

Kovacs

2014

Physiological Reviews

211

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: 87%

“…PTH increases not only with ablation of one or both alleles of Casr (336,340), but in response to EDTA-induced hypocalcemia in fetal lambs (631), calves (715), and rhesus monkeys (524). However, a second study in rhesus monkeys found no increase in fetal PTH in response to EDTAinduced hypocalcemia (189).…”

Section: Pthmentioning

confidence: 97%

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

Kovacs

2014

Physiological Reviews

211

188

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“…The effects of EDTA During early human neonatal life, blood sugar regulation is infusions on fetal serum ionized calcium and parathormone levels incompletely developed and hypoglycemia may occur (28). This is were examined during the hour preceding delivery (12). In all particularly frequent in infants from diabetic mothers requiring experiments, serum ionized calcium, plasma glucose levels, exogenous insulin (6,21,22,24,25).…”

Section: Animalsmentioning

confidence: 99%

Glucose Regulation by Isolated Near Term Fetal Monkey Liver

et al. 1975

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ExtractNear term fetal monkey livers were perfused with a closed recirculating system and a defined perfusion medium. Livers from normal fetal animals were able to release glucose rapidly into the perfusate when they were exposed to glucagon, cyclic AMP, or an aglycemic perfusate, but they did not remove glucose rapidly from the perfusate, synthesize glycogen, or activate liver glycogen synthetase in response to hyperglycemia (Figs. 1,2, and 3; Table I ). Insulin decreased glucose mobilization in response to aglycemia, but did not stimulate glucose uptake during hyperglycemia; insulin activated glycogen synthetase (Table 1; Figs. 1 and 3). Livers from fetuses of streptozotocin-treated mothers and livers from 2-week-old neonates released more glucose into the perfusate in response to aglycemia then did livers from normal fetal monkeys (Fig. 4). These observations support the possibility that neonatal monkey liver is capable of rapidly mobilizing glucose during periods of hypoglycemia but is unable to take up glucose and store glycogen rapidly during periods of hyperglycernia. SpeculationIncomplete development of glycogen synthetic mechanisms in early postnatal life may contribute to decreased liver glycogen reserves. These decreased reserves may then be inadequate for maintaining normoglycemia during periods of increased glucose uptake or utilization by peripheral tissue. (9,10,27,29) support the possibility that at birth hormonal regulation of glycogen metabolism is competent, but direct glucose regulation of glycogen synthesis has not developed.In humans, development of rapid glucose and glycogen mobilizing responses precedes birth (1, 13, 26), and liver glycogen levels, high at birth, decline rapidly during the first few hours of life (3,28). Idiopathic neonatal hypoglycemia does not appear to be associated with impaired glycogenolytic mechanisms since it usually occurs when liver glycogen stores are depleted (3, 28). Consequently, we considered that incomplete development of glycogen synthetic mechanisms in early postnatal life might contribute to decreased liver glycogen reserves and that these inadequate reserves are incapable of maintaining normoglycemia.We now provide additional support for this possibility based on studies with isolated perfused rhesus monkey livers from near term fetuses of normal mothers and mothers with streptozotocin-induced glucose intolerance, and from normal monkey neonates. In all three groups, hepatic glucose removal rates were low in the presence of high glucose concentrations in the perfusion solution. Changes in circulating glucose concentration did not modify glycogen synthetase activity, but in all instances liver glucose was released in response to hypoglycemia. Direct effects of exogenous glucagon and insulin on hepatic glucose output and glycogen cycle enzyme activity were demonstrated in the near term fetus group. METHODS ANIMALSOne of the primary functions for liver is to maintain blood glucose levels. This is achieved by changes in gluconeogenic Pregnant Macaca mulatt...

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25-Hydroxyvitamin D

Fleischman¹

1978

Arch Intern Med

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Perinatal Primate Parathyroid Hormone Metabolism

Cited by 17 publications

References 10 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

Glucose Regulation by Isolated Near Term Fetal Monkey Liver

25-Hydroxyvitamin D

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