Immunoreactive calcitonin content in foetal thyroid glands and in placentae of rats

Jarząb, Barbara; Kokot, F; Bałdys, A

doi:10.1530/acta.0.1050567

Cited by 4 publications

(3 citation statements)

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“…Placenta may be one of the sources of circulating calcitonin in the fetus. In the rat, placental calcitonin levels were higher than serum values and decreased over the last half of gestation, findings consistent with placental elaboration [9]. The decrease in cord blood calcitonin levels with gestation may be accounted for by the decrease in the placental elaboration of calcitonin.…”

Section: Discussionsupporting

confidence: 61%

Cord blood levels of calcium-regulating hormones and osteocalcin in premature infants

Seki¹,

Furuya²,

Makimura³

et al. 1994

Jpme

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We measured cord blood levels of calcium-regulating hormones and osteocalcin in 34 premature infants of various gestational ages. 1,25(OH)2D levels were low in mid-gestation and increased with advancing gestation. Parathyroid hormone levels were low, and calcitonin levels were high in mid-gestation. Both of them declined with advancing gestation. Osteocalcin levels were high in mid-gestation. They increased from 22 weeks through 27 weeks of gestational age, and decreased thereafter. Circulating osteocalcin is considered as a clinical marker of bone turnover. However, cord blood osteocalcin decreased between 27 and 36 weeks of gestation during which period calcium accumulation by the fetus increases. Therefore, cord blood osteocalcin does not appear to reflect fetal bone formation.

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Section: Discussionsupporting

confidence: 61%

Cord blood levels of calcium-regulating hormones and osteocalcin in premature infants

Seki¹,

Furuya²,

Makimura³

et al. 1994

Jpme

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“…Thyroid C-cells and calcitonin are detectable as early as the 30th day of an approximate 145-day gestation in fetal lambs (292), whereas in fetal mice and rats C-cells and calcitonin do not appear until day 15.5 or later out of a gestational period that lasts 19 -22 days, respectively (22,203,284,474,645,679). Near term, fetal calcitonin concentrations are maintained at higher concentrations than in the maternal circulation in rodents (201,430) and lambs (201,204).…”

Section: Calcitoninmentioning

confidence: 99%

“…Calcitonin within the fetal circulation must derive from fetal sources because maternal calcitonin does not cross the rat or mouse placenta (212,430). Rat and mouse placentas also express calcitonin mRNA and protein (284,293,337). The high circulating concentration of calcitonin may occur in response to the increased serum and ionized calcium that is normally present in the fetal circulation.…”

Section: Calcitoninmentioning

confidence: 99%

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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Osteochondrosis in fetuses of ewes overfed calcium

et al. 1991

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Ewes were fed ad libitum (up to maximum of 2.5 kg/day) a complete feed containing either 1.52% calcium (High Ca) or 0.59% calcium (Normal Ca) on a dry matter basis from day 50 of pregnancy, and the fetuses were removed at 133-135 days. Thyroid C cells, identified by indirect immunofluorescence, were more numerous (P less than 0.001) and plasma levels of 24,25-dihydroxycholecalciferol [24,25(OH)2D] were higher (P less than 0.09) in fetuses of High Ca ewes. These fetuses also had retarded cartilage differentiation in the proximal humeral epiphysis and metaphysis as well as transverse trabeculation in the epiphysis. These entities are two of the hallmarks of osteochondrosis. It was shown that feeding high dietary calcium to pregnant ewes caused osteochondrosis in their fetuses. Hypercalcitoninism and/or an adverse effect of supraphysiological levels of 24,25-dihydroxycholecalciferol may have been contributory to the skeletal abnormalities.

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Immunoreactive calcitonin content in foetal thyroid glands and in placentae of rats

Cited by 4 publications

References 0 publications

Cord blood levels of calcium-regulating hormones and osteocalcin in premature infants

Cord blood levels of calcium-regulating hormones and osteocalcin in premature infants

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

Osteochondrosis in fetuses of ewes overfed calcium

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