Mineral transport across the placenta.

Husain, Shahid; Mughal, M Z

doi:10.1136/adc.67.7_spec_no.874

Cited by 43 publications

(15 citation statements)

References 43 publications

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“…Ca 2+ ion is not only known as a secondary messenger, but also as a foremost mineral that is essential to proper fetal development [24]. In the trophoblast, free cytosolic Ca 2+ levels are maintained at a low level compared to maternal blood [25] to facilitate transport of Ca 2+ via the epithelial layer from the maternal circulation to the fetus. In previous studies, most research focused on the transcellular transport pathway but not the paracellular pathway.…”

Section: Discussionmentioning

confidence: 99%

Placental claudin expression and its regulation by endogenous sex steroid hormones

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Placental claudin expression and its regulation by endogenous sex steroid hormones

et al. 2015

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“…The human fetus contains ~16–30 g of phosphorus at birth, with the majority obtained at the time of bone growth during late gestation [2,3]. Despite the rapid cell division, extensive protein signaling, bone development, and other phosphate-dependent processes that occur during this time in development, maternal to fetal phosphate transport mechanisms remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Slc20a2 deficiency results in fetal growth restriction and placental calcification associated with thickened basement membranes and novel CD13 and lamininα1 expressing cells

Wallingford

Gammill

Giachelli

2016

Reproductive Biology

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The essential nutrient phosphorus must be taken up by the mammalian embryo during gestation. The mechanism(s) and key proteins responsible for maternal to fetal phosphate transport have not been identified. Established parameters for placental phosphate transport match those of the type III phosphate transporters, Slc20a1 and Slc20a2. Both members are expressed in human placenta, and their altered expression is linked to preeclampsia. In this study, we tested the hypothesis that Slc20a2 is required for placental function. Indeed, complete deficiency of Slc20a2 in either the maternal or embryonic placental compartment results in fetal growth restriction. We found that Slc20a2 null mice can reproduce, but are subviable; ~50% are lost prior to weaning age. We also observed that 23% of Slc20a2 deficient females develop pregnancy complications at full term, with tremors and placental abnormalities including abnormal vascular structure, increased basement membrane deposition, abundant calcification, and accumulation of novel CD13 and lamininα1 positive cells. Together these data support that Slc20a2 deficiency impacts both maternal and neonatal health, and Slc20a2 is required for normal placental function. In humans, decreased levels of placental Slc20a1 and Slc20a2 have been correlated with early onset preeclampsia, a disorder that can manifest from placental dysfunction. In addition, preterm placental calcification has been associated with poor pregnancy outcomes. We surveyed placental calcification in human preeclamptic placenta samples, and detected basement membrane-associated placental calcification as well as a comparable lamininα1 positive cell type, indicating that similar mechanisms may underlie both human and mouse placental calcification.

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“…In pregnancy, especially in the third trimester, inorganic phosphorus moves from the mother to the fetus against a concentration gradient (Brunette et al, 1986;Husain and Mughal, 1992). This is a sodium-dependent, energy-requiring process facilitated by NaPi-IIb (SLC34A2) transporters, which are expressed in the placental labyrinthine cells (Mitchell and Jüppner, 2010).…”

Section: Distribution To Tissuesmentioning

confidence: 99%

Scientific Opinion on Dietary Reference Values for phosphorus

Products¹

2015

EFS2

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Following a request from the European Commission, the Panel on Dietetic Products, Nutrition and Allergies derived Dietary Reference Values (DRVs) for phosphorus. The Panel considered data from balance studies, losses of phosphorus from the body and intestinal absorption for possible use in a factorial approach, and studies on phosphorus intake and long-term health outcomes. The Panel concluded that these data were insufficient for setting DRVs for phosphorus. Data on the calcium to phosphorus ratio in bones of healthy adults, adjusted for the proportion of phosphorus found outside bone, and data on whole-body calcium and phosphorus contents in Caucasian adults indicate that the calcium to phosphorus molar ratio in the body ranges from 1.4:1 to 1.9:1. Although the fractional absorption of phosphorus is higher than that of calcium, the Panel considered that the actual amounts of calcium and phosphorus that are available for absorption from the diet cannot be determined; therefore, the whole-body calcium to phosphorus ratio was used to set DRVs. The data were considered insufficient to derive Average Requirements and Population Reference Intakes. Based on the DRVs for calcium and considering a molar calcium to phosphorus ratio of 1.4:1 to 1.9:1, amounts of phosphorus were calculated. The Panel chose the lower bound of this range (a ratio of 1.4:1, which results in a higher phosphorus intake value) for setting an Adequate Intake (AI), taking into account estimated phosphorus intakes in Western countries, which are considerably higher than the values calculated. The AI is 160 mg/day for infants (7-11 months) and between 250 and 640 mg/day for children. For adults, the AI is 550 mg/day. Taking into consideration adaptive changes in phosphorus metabolism that occur during pregnancy and lactation, it was considered that the AI for adults also applies to pregnant and lactating women. Phosphorus is involved in many physiological processes, such as in the cell's energy cycle, in regulation of the body's acid-base balance, as a component of the cell structure, in cell regulation and signalling, and in the mineralisation of bones and teeth. About 85 % of the body's phosphorus is in bones and teeth, 14 % is in soft tissues, including muscle, liver, heart and kidney, and only 1 % is present in extracellular fluids. Phosphorus homeostasis is intricately linked to that of calcium because of the actions of calcium-regulating hormones, such as parathyroid hormone (PTH) and 1,25-dihydroxy-vitamin D (1,25(OH) 2 D), at the level of the bone, the gut and the kidneys. © EuropeanPhosphorus absorption occurs through passive diffusion and sodium-dependent active transport and via paracellular and cellular pathways. In adults, limited data suggest that net phosphorus absorption ranges from 55 to 80 % of intake. Phosphorus absorption is affected by the total amount of phosphorus in the diet and also by the type of phosphorus (organic versus inorganic), the food origin (animalversus plant-derived) and the ratio of phosphorus to oth...

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Mineral transport across the placenta.

Cited by 43 publications

References 43 publications

Placental claudin expression and its regulation by endogenous sex steroid hormones

Placental claudin expression and its regulation by endogenous sex steroid hormones

Slc20a2 deficiency results in fetal growth restriction and placental calcification associated with thickened basement membranes and novel CD13 and lamininα1 expressing cells

Scientific Opinion on Dietary Reference Values for phosphorus

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