Elevated 1,25-dihydroxyvitamin D plasma levels in normal human pregnancy and lactation.

Kumar, Rajiv; Cohen, Wayne R.; Silva, Patrícia Cristina Lisbôa da; Epstein, Franklin H.

doi:10.1172/jci109308

Cited by 307 publications

(106 citation statements)

References 17 publications

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“…In contrast, an increase in plasma 1,25-dihydroxyvitamin D (1,25(OH) 2 D) concentration is apparent in the first trimester in studies using NPNL women as reference (67,144,145,174) . Plasma concentrations of 1,25(OH) 2 D continue to rise during pregnancy, and in late pregnancy are several-fold higher than before pregnancy (67,144) and early gestation (60,67,107,112,144,145,174 -178) .…”

Section: Regulation Of Calcium Metabolism In Pregnancy and Lactationmentioning

confidence: 99%

“…However, because PTH concentration is lowered or unchanged in pregnant women, it is unlikely to be primarily responsible for the increase in 1,25(OH) 2 D seen in pregnancy (3) , although it remains responsive to changes in Ca load (147) . Although hormones, such as oestrogen, prolactin, growth hormone and insulin-like growth factor-I, have the ability to induce 1-a-hydroxylase activity (174,175,181) , it is likely that PTHrP has a key role (3,179,182) . This activates the PTH/PTHrP receptor and therefore exhibits PTH-like effects, including stimulation of renal 1,25(OH) 2 D production (182,183) .…”

Section: Regulation Of Calcium Metabolism In Pregnancy and Lactationmentioning

confidence: 99%

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Calcium economy in human pregnancy and lactation

et al. 2012

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Pregnancy and lactation are times of additional demand for Ca. Ca is transferred across the placenta for fetal skeletal mineralisation, and supplied to the mammary gland for secretion into breast milk. In theory, these additional maternal requirements could be met through mobilisation of Ca from the skeleton, increased intestinal Ca absorption efficiency, enhanced renal Ca retention or greater dietary Ca intake. The extent to which any or all of these apply, the underpinning biological mechanisms and the possible consequences for maternal and infant bone health in the short and long term are the focus of the present review. The complexities in the methodological aspects of interpreting the literature in this area are highlighted and the inter-individual variation in the response to pregnancy and lactation is reviewed. In summary, human pregnancy and lactation are associated with changes in Ca and bone metabolism that support the transfer of Ca between mother and child. The changes generally appear to be independent of maternal Ca supply in populations where Ca intakes are close to current recommendations. Evidence suggests that the processes are physiological in humans and that they provide sufficient Ca for fetal growth and breast-milk production, without relying on an increase in dietary Ca intake or compromising long-term maternal bone health. Further research is needed to determine the limitations of the maternal response to the Ca demands of pregnancy and lactation, especially among mothers with marginal and low dietary Ca intake, and to define vitamin D adequacy for reproductive women.

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Section: Regulation Of Calcium Metabolism In Pregnancy and Lactationmentioning

confidence: 99%

Section: Regulation Of Calcium Metabolism In Pregnancy and Lactationmentioning

confidence: 99%

Calcium economy in human pregnancy and lactation

et al. 2012

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“…Gestational age clearly influences mineral metabolism in both mother and fetus. The fetus produces 1,25-dihydroxyvitamin D and hence regulates its own active calcium uptake across the placenta (26,38). The most active phase of calcium transfer to the fetus occurs in the last trimester of pregnancy, a period that coincides with the critical phases of neurodevelopment in which synaptogenesis and arborization ofthe cortex and cerebellum occur (39).…”

Section: Important Factors In Bone Lead Mobilizationmentioning

confidence: 99%

Lead in bone: implications for toxicology during pregnancy and lactation.

Silbergeld

1991

Environ Health Perspect

267

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Advances in understanding the distribution and retention of lead in mineralized tissues are important for two reasons: first, bone lead may be a more accurate dosimeter of integrated absorption associated with chronic exposures, and second, bone lead may be a source of internal exposure to the host organism. Little attention has been paid to this second aspect, the remobilization of lead from bone. Mobilization of lead from bone is likely to occur during periods of altered mineral metabolism; since calciotropic factors determine the uptake and storage of lead in this compartment, changes in calcium-related regulatory factors are likely to affect lead compartmentation. Calcium metabolism changes drastically in humans during pregnancy and lactation; although relatively little is known of lead kinetics during these critical periods, it is likely that bone lead is mobilized and transferred to the more bioavailable compartment of the maternal circulation, with potential toxic effects on the fetus and the mother.

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“…These rats received 25(OH)[3H]D3 as described below. Additionally, plasma was obtained from 10 vitamin D-deplete rats raised for 7 weeks on the diet described above and used for measurement of 25(OH)D3 and 1,25(OH)2D3 levels by described methods (8,22,23). Another group of eight rats received 10 Twenty-four hours after the injection of 25(OH)[3H]D3, rats were exsanguinated and plasma was separated from the blood cells.…”

Section: Gray Et Al (5) Administeredmentioning

confidence: 99%

Do tissues other than the kidney produce 1,25-dihydroxyvitamin D3 in vivo? A reexamination.

Shultz¹,

Fox²,

Heath³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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Recent experiments have shown that 1,25-dihydroxyvitamin D3-like material is produced in cultured nonrenal cells and may be present in the sera of anephric patients. We reexamined the question of whether 1,25-dihydroxyvitamin D3 can be synthesized extrarenally in the rat in vivo. To intact, sham-operated, ureter-ligated, or acutely nephrectomized vitamin D-deficient rats raised on a diet normal in calcium and phosphorus, we gave a physiologic dose of high-specific-activity 25-hydroxy-[3H]vitaminD3(3.6-3.81uCi; -25pmolper rat). Twenty-fourhours later we examined their tissues and plasma for the presence of radiolabeled 1,25-dihydroxyvitamin D3. Large amounts of radioactivity that behaved chromatographically as identical with authentic 1,25-dihydroxyvitamin D3 were present in the plasma, bone, and intestine of the intact, sham-operated, or ureter-ligated rats. However, no radioactivity eluting in a manner similar to 1,25-dihydroxyvitamin D3 was found in plasma, bone, or intestine of acutely nephrectomized rats. We conclude that, in the acutely nephrectomized living rat, 1,25-dihydroxyvitamin D3 is not present in plasma, bone, or intestine in quantities detectable by the sensitive techniques we have used. No conversion of 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 was observed during a 24-hr period after nephrectomy of vitamin D-deprived rats. This fact casts doubt upon the significance of the in vitro production of 1,25-dihydroxyvitamin D3 by nonrenal cells as an in vivo phenomenon. Gray et al. (3), found that radiolabeled 1,25(OH)2D3 was absent from the tissues and plasma of acutely nephrectomized rats that had received low-specific-activity radiolabeled vitamin D3 or 25(OH)D3 immediately after nephrectomy. In human anephric subjects given radiolabeled vitamin D3, Mawer et aL (4) failed to detect radioactive 1,25(OH)2D3. Gray et al. (5) administered 25(OH)[3H]D3to 10 anephric subjects; in none of the patients studied was radiolabeled 1,25(OH)2D3 detected. In these human studies, radiolabeled 1,25(OH)2D3 was clearly detectable in normal subjects (4, 5). Lambert et al. (6) found recently that a substance was present in the plasma ofanephric subjects that displaced 1,25(OH)2[3H]D3 from its receptor; additionally, samples processed in a similar manner displaced 45Ca from labeled fetal bone in a bioassay system for 1,25(OH)2D3. The authors concluded that 1,25(OH)2D3 was present in the plasma of anephric subjects. However, other investigators, using radioreceptor, radioimmune, and biological assays for 1,25(OH)2D3, have been unable to detect 1,25(OH)2D3 in anephric persons (7-12).In certain situations, however, 1,25(OH)2D3 may be synthesized extrarenally. For example, a report by Barbour et al. (13) showed that an anephric subject with sarcoidosis had detectable plasma 1,25(OH)2D3-like material at a time when he was hypercalcemic (13)

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Elevated 1,25-dihydroxyvitamin D plasma levels in normal human pregnancy and lactation.

Cited by 307 publications

References 17 publications

Calcium economy in human pregnancy and lactation

Calcium economy in human pregnancy and lactation

Lead in bone: implications for toxicology during pregnancy and lactation.

Do tissues other than the kidney produce 1,25-dihydroxyvitamin D3 in vivo? A reexamination.

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