Vitamin A Transfer to the Fetus and to the Amniotic Fluid in Rhesus Monkey &lt;i&gt;(Macaca mulatto)&lt;/i&gt;

Vahlquist, Anders; Nilsson, Sten

doi:10.1159/000176840

Cited by 28 publications

(7 citation statements)

References 34 publications

(50 reference statements)

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“…The mechanisms of transplacental flux of vitamin A are still not well-understood. Studies in rat (139) and monkey (144) have indicated that maternal retinol-binding protein crosses the placenta. The human placenta expresses surface receptors that bind retinolbinding protein (141), and the transplacental flux of the retinol-binding protein complex may be the main pathway for vitamin A transport across the placenta early in pregnancy.…”

Section: Lipid-soluble Vitaminsmentioning

confidence: 99%

“…Fetal retinol-binding protein production occurs later in gestation (139). A second proposed mechanism for placental vitamin A transport is that the maternal retinol-binding protein binds to its receptor and releases retinol into the syncytiotrophoblast without the protein being internalized (144). The placenta then forms a retinyl ester that is secreted into the fetal circulation as lipoprotein.…”

Section: Lipid-soluble Vitaminsmentioning

confidence: 99%

See 1 more Smart Citation

Nutrient Transport Pathways Across the Epithelium of the Placenta

Smith¹,

Moe²,

Ganapathy³

1992

Annu. Rev. Nutr.

113

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Section: Lipid-soluble Vitaminsmentioning

confidence: 99%

Section: Lipid-soluble Vitaminsmentioning

confidence: 99%

Nutrient Transport Pathways Across the Epithelium of the Placenta

Smith¹,

Moe²,

Ganapathy³

1992

Annu. Rev. Nutr.

113

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“…Vitamin-A deficiency results in a predictable se quence of progressive changes in the epithe lial lining of pulmonary conducting airways [1][2][3]. These changes, classically described as necrotizing tracheobronchitis in early stages and squamous metaplasia in more advanced stages of the deficiency, are reversible with restoration of normal vitamin A status [4], Studies in various animal species have shown a transfer of vitamin A from mother to fetus during pregnancy, particularly in late gestation [5][6][7][8][9][10][11]. Although as much as 90% of total body reserve of vitamin A is found in the liver [12], it is suggested that other organs, including the developing lungs, may be capable of vitamin-A uptake, esteri fication, and storage [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Effect of Maternal Vitamin-A Administration on Fetal Lung Vitamin-A Stores in the Perinatal Rat

Shenai¹,

Chytil²

1990

Neonatology

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Vitamin A (retinol) is essential for normal differentiation and integrity of developing respiratory epithelium and its deficiency has been linked to an increased susceptibility to lung injury. Because significant vitamin-A storage occurs in the fetal lung near term in the perinatal rat, prematurely born animals deprived of adequate stores in their lungs may be susceptible to the adverse effects of vitamin-A deficiency. It would be desirable if lung vitamin-A stores could be augmented with maternal administration, but the feasibility of this strategy has not been reported. We therefore conducted this study in rats to determine whether maternal administration of vitamin A could increase the lung stores of vitamin A in the offspring. Vitamin-A-sufficient pregnant rats were given a single dose of either vitamin A (50,000 IU retinyl palmitate) or 0.9% saline solution on gestational day 16 (term = 21 days) by the intragastric route. High-performance liquid chromatography was used to measure concentrations of vitamin A and its esters in fetal and neonatal lungs and livers at times ranging from gestational day 17 through 21, and from postnatal day 1 through 14. The concentrations of vitamin-A esters in the lungs of fetuses and newborn pups of the vitamin-A-treated animals were significantly (1.7- to 7.1-fold) higher than those of the control group. This increase in the lung vitamin-A ester concentrations was seen within 24 h of maternal administration and persisted throughout the 14-day postnatal period. Maternal administration of vitamin A was also associated with an increase in the liver vitamin-A ester concentrations in the offspring, although this increase was less in magnitude and duration relative to the increase in the lung vitamin-A ester concentrations. We conclude that a prompt, sustained increase in the fetal lung stores of vitamin A is possible following prenatal administration of a single large dose of vitamin A to the mother. The possibility that vitamin-A administration to human mothers with imminent preterm deliveries might augment the lung vitamin-A stores of their newborn infants at birth needs to be explored.

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“…This question has been approached in animal models (sheep, mouse, monkey), but the placental metabolism of retinoids is difficult to deduce from studies in the intact animal, and extrapolation of these results to humans is uncertain (11)(12)(13). Measurements of human placental, maternal, and cord retinoid concentrations have been reported, but they shed little light on the metabolic pathway (14,15).…”

mentioning

confidence: 99%

Esterification of Vitamin A by the Human Placenta Involves Villous Mesenchymal Fibroblasts

et al. 2000

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Vitamin A (retinol) and its active derivatives (retinoic acids) are essential for growth and development of the mammalian fetus. Maternally derived retinol must pass the placenta to reach the developing fetus. Despite its apparent importance, little is known concerning placental transfer and metabolism of retinol, and particularly of placental production and storage of retinyl esters. To elucidate this metabolic pathway, we incubated, in the presence of retinol, 1) human full-term placental explants and 2) primary cultures of major cells types contributing to placental function: trophoblasts and villous mesenchymal fibroblasts. We used HPLC to determine the types and concentrations of retinyl esters produced by these explants and cells. About 14% of total cellular retinol in placental explants was esterified. The most abundant esters were myristate and palmitate. Primary cell cultures showed that fibroblasts efficiently produced retinyl esters, but trophoblasts did not. In both types of experiments, no retinyl esters were detected in the culture medium, suggesting that retinyl esters were produced for storage purpose. These results suggest that villous mesenchymal fibroblasts are primary sites of retinol esterification and storage in the placenta. In addition to their essential roles in vision, growth, and maintenance of differentiated epithelia, vitamin A (retinol) and its active derivatives, the RAs, are required for normal mammalian reproduction and fetal development (1, 2). Maternal vitamin A deficiency can result in fetal death or in a spectrum of malformations, the fetal vitamin A deficiency syndrome (3-6). Excessive vitamin A intake can also produce a spectrum of congenital defects, in a dose-and developmental stagedependent manner (7,8). Because there is no de novo fetal synthesis of retinol, the developing mammalian embryo is dependent on the maternal circulation for its vitamin A intake. The presence of measurable hepatic vitamin A stored at birth is indicative of the functionality and importance of placental transport during pregnancy (9, 10). Abnormalities of placental transfer could have serious consequences on fetal development and integrity.Despite its apparent importance, little is known about placental transfer and metabolism of retinoids. This question has been approached in animal models (sheep, mouse, monkey), but the placental metabolism of retinoids is difficult to deduce from studies in the intact animal, and extrapolation of these results to humans is uncertain (11-13). Measurements of human placental, maternal, and cord retinoid concentrations have been reported, but they shed little light on the metabolic pathway (14,15). Experiments using human perfused placenta and full-term human placental tissues in vitro have yielded controversial results concerning retinoid metabolism, especially the ability of the placenta to produce and store retinyl esters from retinol (16,17).To better characterize retinoid metabolism, we have investigated placental capacity to esterify retinol into retinyl es...

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Vitamin A Transfer to the Fetus and to the Amniotic Fluid in Rhesus Monkey <i>(Macaca mulatto)</i>

Cited by 28 publications

References 34 publications

Nutrient Transport Pathways Across the Epithelium of the Placenta

Nutrient Transport Pathways Across the Epithelium of the Placenta

Effect of Maternal Vitamin-A Administration on Fetal Lung Vitamin-A Stores in the Perinatal Rat

Esterification of Vitamin A by the Human Placenta Involves Villous Mesenchymal Fibroblasts

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