Knowledge needed about the exchange physiology of the placenta

Sibley, Colin P.; Brownbill, Paul; Glazier, Jocelyn D.; Greenwood, Susan

doi:10.1016/j.placenta.2018.01.006

Cited by 34 publications

(21 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As described in detail elsewhere [ 23 , 28 ], the rate of transfer across the placenta of an inert uncharged solute is described by Fick’s Law of diffusion and gives a measure of the passive permeability. Thus, flux is determined directly by the surface area for exchange and the maternal–fetal concentration gradient, and inversely by the thickness of the barrier and the size of the molecule (usually determined by its diffusion coefficient in water at 37 °C).…”

Section: Discussionmentioning

confidence: 99%

“…Heterogenous channel populations in the hemochorial placenta have previously been suggested [ 31 ]. As discussed in [ 28 ], the nature of the diffusional route for hydrophilic solutes across the placenta is a fundamental piece of information lacking in our understanding of placental exchange physiology; the Phlda2 −/+ mutant might provide a useful tool for dissecting the nature and regulation of this route.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Deletion of the Imprinted Phlda2 Gene Increases Placental Passive Permeability in the Mouse

Angiolini

Sandovici

Coan

et al. 2021

Genes

Self Cite

View full text Add to dashboard Cite

Genomic imprinting, an epigenetic phenomenon that causes the expression of a small set of genes in a parent-of-origin-specific manner, is thought to have co-evolved with placentation. Many imprinted genes are expressed in the placenta, where they play diverse roles related to development and nutrient supply function. However, only a small number of imprinted genes have been functionally tested for a role in nutrient transfer capacity in relation to the structural characteristics of the exchange labyrinthine zone. Here, we examine the transfer capacity in a mouse model deficient for the maternally expressed Phlda2 gene, which results in placental overgrowth and a transient reduction in fetal growth. Using stereology, we show that the morphology of the labyrinthine zone in Phlda2−/+ mutants is normal at E16 and E19. In vivo placental transfer of radiolabeled solutes 14C-methyl-D-glucose and 14C-MeAIB remains unaffected at both gestational time points. However, placental passive permeability, as measured using two inert hydrophilic solutes (14C-mannitol; 14C-inulin), is significantly higher in mutants. Importantly, this increase in passive permeability is associated with fetal catch-up growth. Our findings uncover a key role played by the imprinted Phlda2 gene in modifying placental passive permeability that may be important for determining fetal growth.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Deletion of the Imprinted Phlda2 Gene Increases Placental Passive Permeability in the Mouse

Angiolini

Sandovici

Coan

et al. 2021

Genes

Self Cite

View full text Add to dashboard Cite

show abstract

“…In fact, transporter proteins are located in the plasma membrane along with carriers, which are membrane proteins as well. The purpose of the carriers is to merge themselves with the solute and transport the solute to other parts of the membrane, similarly to the transporter proteins [20,21]. The functionalities and system of exchange of fluids across the placental barrier is an important part of the placenta.…”

Section: Human Placentamentioning

confidence: 99%

Drug transport across the human placenta: review of placenta-on-a-chip and previous approaches

2019

View full text Add to dashboard Cite

One contribution of 15 to a theme issue 'Bioengineering in women's health, volume 2: pregnancy-from implantation to parturition'.In the past few decades, the placenta became a very controversial topic that has had many researchers and pharmacists discussing the significance of the effects of pharmaceutical drug intake and how it is a possible leading cause towards birth defects. The creation of an in vitro microengineered model of the placenta can be used to replicate the interactions between the mother and fetus, specifically pharmaceutical drug intake reactions. As the field of nanotechnology significantly continues growing, nanotechnology will become more apparent in the study of medicine and other scientific disciplines, specifically microengineering applications. This review is based on past and current research that compares the feasibility and testing of the placenta-on-a-chip microengineered model to the previous and underdeveloped in vivo and ex vivo approaches. The testing of the practicality and effectiveness of the in vitro, in vivo and ex vivo models requires the experimentation of prominent pharmaceutical drugs that most mothers consume during pregnancy. In this case, these drugs need to be studied and tested more often. However, there are challenges associated with the in vitro, in vivo and ex vivo processes when developing a practical placental model, which are discussed in further detail.

show abstract

“…Considering that fetal growth is primarily determined by nutrient availability, which is intimately related to placental nutrient transport [12,13], we hypothesize the changes in placenta caused by dietary Leu supplementation might be the main contribution to the improved nutrient supplying from maternal to fetus and then effect on fetal development. Nutrients in maternal circulation were accumulated in placenta via speci c transporters and then some of them are metabolized within placenta to supply energy for organ development and maintenance or converted to other active substance which could regulate placental function within placenta or further transported to fetal circulation.…”

Section: Introductionmentioning

confidence: 99%

Leucine supplementation during late gestation globally altered placental metabolism and nutrient transport via modulation of the PI3K/AKT/mTOR signalling pathway

Cui

Zhu

et al. 2021

Preprint

View full text Add to dashboard Cite

Background Our previous study found that sow dietary leucine supplementation signicicantly improved fetal intrauterine growth and newborn piglet birth weight. But we still have limited knowledge how leucine regulated placental functions to promote the nutrient supply to fetus to support its intrauterine development. Methods 150 sows at day 90 of gestiation were divided into three groups and fed with either control diet (CON), CON + 0.4% Leu or CON + 0.8% Leu separately until parturition. Placental metabolomics, full spectrum amino acids and nutrient transporters were systematically analyzed. Results Leu supplementation lead to an altered placental metabolism with higher amount of metabolites related to glycolysis and fatty acids oxidatation, and more amino acids accumulation in placenta. Besides, nutrient transporters including amino acids transporters, glucose transporters and fatty acids transporters in placenta were globally enhanced and several enzymes related to energy metabolism including hexokinase, succinatede hydrogenase, lactated hydrogenase, glycogen phosphorylase and hydroxyaryl-CoA-dehydrogenase were significantly increased with no change in antioxidative status in the groups with Leu supplementation. Futhermore, Leu supplementation significantly increased phosphalation of PI3K, Akt, and mTOR in placenta compared with control group. Conclusions Leu supplementation during late gestation globally altered placental metabolism, nutrient transport (amino acids, glucose, and fatty acids) via modulation of the PI3K/Akt/mTOR signalling pathway.

show abstract

Knowledge needed about the exchange physiology of the placenta

Cited by 34 publications

References 37 publications

Deletion of the Imprinted Phlda2 Gene Increases Placental Passive Permeability in the Mouse

Deletion of the Imprinted Phlda2 Gene Increases Placental Passive Permeability in the Mouse

Drug transport across the human placenta: review of placenta-on-a-chip and previous approaches

Leucine supplementation during late gestation globally altered placental metabolism and nutrient transport via modulation of the PI3K/AKT/mTOR signalling pathway

Contact Info

Product

Resources

About