scholarly journals Foetal glutamate as a possible precursor of placental glutamine in the guinea pig

1981 ◽  
Vol 198 (2) ◽  
pp. 397-401 ◽  
Author(s):  
D L Bloxam ◽  
C F Tyler ◽  
M Young

The role of foetal glutamate as a source of placental glutamine was investigated in the near-term pregnant guinea-pig placenta perfused in situ through the umbilical vessels. With normal foetal amino acid concentrations there was a significant two-way exchange of glutamate between the placenta and foetal perfusate, but a net release of the amino acid from the placenta. Radioactively labelled glutamate carbon entering the placenta by this exchange was freely incorporated into intracellular glutamine, but only 1.5% of it was found in glutamine transported out into the foetal circulation. In the guinea pig, therefore, foetal glutamate does not appear to be a precursor of glutamine released from the placenta on the foetal side.

2005 ◽  
Vol 191 (11) ◽  
pp. 1889-1897 ◽  
Author(s):  
Anna I. Bakardjiev ◽  
Brian A. Stacy ◽  
Daniel A. Portnoy

Neonatology ◽  
1977 ◽  
Vol 32 (1-2) ◽  
pp. 1-4 ◽  
Author(s):  
Enid Fenton

2021 ◽  
Vol 5 (7) ◽  
pp. 01-06
Author(s):  
Sing-yung Wu ◽  
Charles H. Emerson ◽  
Edward Tjioe ◽  
Dong-bao Chen

Objective: Serum 3, 3’,5-triiodothyronine (T3) remains low in near-term fetus to prevent the growing fetus from undue exposure to its active catabolic effect in mammals. The present study was undertaken to gain insight in the role of placenta in T3 metabolism, fetal to maternal transfer of T3, and its metabolites by in situ placenta perfusion with outer-ring labeled [125I]-T3 in pregnant guinea pig, a species showing increased sulfated 3, 3’-diiodothyronine (T2S) levels in maternal serum in late pregnancy (term = 65 days), similarly to humans in pregnancy. Materials and Methods: One-pass placenta perfusions performed on pregnant guinea pigs were studied between 58 - 65 days of gestation. In two separate experiments, the umbilical artery of the guinea pig placenta was perfused in situ at 37°C with outer-ring labeled [125I]-T3. Maternal sera and umbilical effluents were obtained for analysis at the end of a 60-minute perfusion, when the steady-state levels of radioactivity were reached in the placenta effluent after 30-minute. Results: Sulfated [125I]-T2S was readily detected in the maternal serum as the major metabolite of T3 following the perfusion of placenta with [125I]-T3, suggesting that placental inner-ring deiodinase and sulfotransferase may play an important role in fetal T3 homeostasis and in the fetal to maternal transfer of sulfated iodothyronine metabolites. Conclusions: The expression of type 3 deiodinase (D3) and thyroid hormone sulfotransferase activity in placenta may play an important role to protect developing organs against undue exposure to active thyroid hormone in late gestation in the fetus. The combined activities of D3 and sulfotransferase promoted a placental transfer of T2S into maternal circulation. The maternal circulation of T2S is fetal T3 in origin and its role as a fetal thyroid function biomarker deserves further evaluations and studies.


1988 ◽  
Vol 254 (6) ◽  
pp. C735-C743 ◽  
Author(s):  
J. H. Sweiry ◽  
D. L. Yudilevich

Trophoblast uptake of folate and methotrexate (MTX) was investigated in an in situ or dually perfused (maternal and fetal side) guinea pig placenta by using a single-circulation, paired-tracer technique. For [3H]folate, uptake into trophoblast was rapid (s), high (60–80%) and Na+ independent, and exhibited negligible efflux on both poles of placenta. [3H]folate uptake could be inhibited by folate or 5-methyltetrahydrofolate (CH3THF) but not by equimolar (0.1 microM) MTX, folinic acid, aminopterin, trimoprim, or adenine when these compounds were present in perfusate. Inhibitory effect of folate was time dependent, and its complete reversal by folate-free perfusion required up to 20 min. This suggests the presence of a high-affinity folate carrier that exhibits a slow rate of self exchange. A sudden (bolus) increase of 10 microM folate of CH3THF caused a 70–80% inhibition of [3H]folate uptake, whereas folinic acid, MTX, and trimoprim were two- to threefold less effective. [3H]folate uptake was insensitive to DIDS, SITS, nicotine, ethanol, or phenytoin. For [3H]MTX, uptake was high (60–80%) on both sides of trophoblast, however, as distinct from [3H]folate, rapid and complete efflux followed the initial uptake. [3H]MTX uptake was not inhibited by 0.1 microM MTX, but equimolar folate or CH3THF were highly effective (90%) inhibitors; higher concentration (1 microM) of MTX reduced [3H]MTX uptake by 58%. Transplacental transfer of [3H]folate or [3H]MTX in excess of the leak pathway marker in either direction was not observed. Inhibition obtained by highly concentrated substrate bolus injections indicates saturation (less than 2 microM) of membrane folate carrier.(ABSTRACT TRUNCATED AT 250 WORDS)


2010 ◽  
Vol 22 (9) ◽  
pp. 57
Author(s):  
P. A. Grant ◽  
K. L. Kind ◽  
A. Sohlstrom ◽  
K. Gatford ◽  
C. T. Roberts ◽  
...  

Functional development of the placenta ensures an adequate supply of nutrients for fetal growth throughout gestation. Placental nutrient transport capacity increases during gestation, through alterations in structure and abundance of its molecular determinants, including expression of Slc2a1 (glucose transporter type-1) and Slc38a2 (system A amino acid transporter), as well as Igf1and Igf2. Each of these genes are predicted targets of microRNAs. Non-coding RNAs can down-regulate, as well as activate translation, by interacting with complementary regions in the promoter, coding, or 3’UTR of target mRNAs.(1) MicroRNAs are present in the mammalian placenta,(2) but little is known about developmental changes in their expression and actions. We hypothesised that placental expression of microRNAs which target molecular mediators of nutrient transport changes during gestation. Expression of microRNAs in the guinea pig placenta was examined at D30 (n = 7) and D60 (n = 7) of gestation (term = D70) by Exiqon microarray. Gene expression was measured by real-time PCR. Predicted gene targets were identified using miRecords and networks and pathways by Ingenuity Pathway Analysis. Placental expression of 119 microRNAs was upregulated (P < 0.05), and that of 40 was down-regulated (P < 0.05), at late compared to early gestation. Of the 20 most abundant differentially up- or down-regulated microRNAs, 11 are predicted to target members of solute carrier families. This includes has-miR-26a (↑2X), which is predicted to target Slc38a2 mRNA and expression of has-miR-26a and Slc38a2 was positively correlated (P < 0.02). Alternate predicted targets of has-miR-26a include networks involving amino acid metabolism, molecular transport and small molecular biochemistry. These findings support the hypotheses that gestational changes in microRNA expression act to regulate functional development of the placenta, including expression of genes that mediate nutrient transport. (1) Breving K, Esquela-Kerscher A. Int J Biochem Cell Biol 2009.(2) Barad O, et al. Genome Res 2004 14: 2486–2494.


Placenta ◽  
1998 ◽  
Vol 19 (7) ◽  
pp. A41
Author(s):  
H.J. Schröder ◽  
M. Tchirikov

1965 ◽  
Vol 208 (3) ◽  
pp. 563-572 ◽  
Author(s):  
Steven Schenker ◽  
Joe Goldstein ◽  
Burton Combes

Unconjugated and conjugated S35-labeled BSP were administered to viable fetal guinea pigs with intact placental circulation. Guinea pig placenta was virtually impermeable to unconjugated and conjugated BSP, thus permitting a comparison of the disposition of both dye compounds in the fetus, and additional comparison with adult guinea pigs receiving comparable weight-adjusted doses of BSP. Although conjugated BSP disappeared more slowly from plasma than unconjugated BSP in fetal and adult animals, it was delivered more rapidly into bile, indicating a shorter hepatic phase for conjugated BSP. The rate of delivery of both dye compounds into bile was considerably decreased in fetal guinea pigs when compared with values in adult animals. Biliary excretion of administered unconjugated BSP was disproportionately depressed, however, indicating that conjugation of BSP was impaired. Excretion of conjugated BSP into bile was also impaired in the fetus. Since conjugation appears to be impaired to a greater extent than excretion of conjugated and unconjugated BSP into bile in near-term fetal guinea pigs, conjugation, rather than excretion, is rate limiting in BSP delivery into bile in these animals.


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