Lactate carriers in the artificially perfused human term placenta

doi:10.1016/S0143-4004(83)80029-0

Placenta

Volume 4, Issue 2, April–June 1983, Pages 165-174

https://doi.org/10.1016/S0143-4004(83)80029-0 Get rights and content

Summary

Thirty-two isolated cotyledons from human term placentae were perfused artificially with a tissue culture medium on the material and the fetal side.

The transfer and uptake of labelled l-lactate and d-lactate (test substance) relative to l-glucose (reference substance, extracellular marker) were investigated in steady-state experiments (n=9) and in a single passage paired tracer dilution technique (n=23).

The l-lactate transfer exceeded the l-glucose transfer two to three times.

The l-lactate uptake into the trophoblast—both from the maternal and the fetal side—was more than three times that of d-lactate. l-lactate transfer and uptake were inhibited by phloretin.

The l-lactate transfer showed a saturation kinetic at increasing chemical concentrations of lactate.

It is concluded that lactate carriers exist both in the maternal and fetal side of the trophoblast.

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Interestingly, however, cardiac lactate concentrations were not significantly affected by adrenergic deficiency. Possible explanations for this finding could be minimal GAPDH activity is compensated by extra-cardiac (including maternal circulation) lactate or other pyruvate sources, such as alanine, glycine, and/or glycerol 3-phosphate (which was not diminished in concentration in adrenergic hormone-deficient hearts, see Fig. 2, heat map), that help maintain lactate concentrations under anaerobic conditions (51–53). This would indicate that adrenergic hormones are necessary to shift the fate of glucose from anaerobic lactate formation to glucose oxidation and aerobic respiration during this phase of embryonic development (embryonic shift) (5).
Cardiac energy demands during early embryonic periods are sufficiently met through glycolysis, but as development proceeds, the oxidative phosphorylation in mitochondria becomes increasingly vital. Adrenergic hormones are known to stimulate metabolism in adult mammals and are essential for embryonic development, but relatively little is known about their effects on metabolism in the embryonic heart. Here, we show that embryos lacking adrenergic stimulation have ∼10-fold less cardiac ATP compared with littermate controls. Despite this deficit in steady-state ATP, neither the rates of ATP formation nor degradation was affected in adrenergic hormone-deficient hearts, suggesting that ATP synthesis and hydrolysis mechanisms were fully operational. We thus hypothesized that adrenergic hormones stimulate metabolism of glucose to provide chemical substrates for oxidation in mitochondria. To test this hypothesis, we employed a metabolomics-based approach using LC/MS. Our results showed glucose 1-phosphate and glucose 6-phosphate concentrations were not significantly altered, but several downstream metabolites in both glycolytic and pentose–phosphate pathways were significantly lower compared with controls. Furthermore, we identified glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase as key enzymes in those respective metabolic pathways whose activity was significantly (p < 0.05) and substantially (80 and 40%, respectively) lower in adrenergic hormone-deficient hearts. Addition of pyruvate and to a lesser extent ribose led to significant recovery of steady-state ATP concentrations. These results demonstrate that without adrenergic stimulation, glucose metabolism in the embryonic heart is severely impaired in multiple pathways, ultimately leading to insufficient metabolic substrate availability for successful transition to aerobic respiration needed for survival.
Mechanisms of Transfer Across the Human Placenta
2017, Fetal and Neonatal Physiology, 2-Volume Set
Amniotic fluid and blood lactate concentrations in mares and foals in the early postpartum period
2012, Theriogenology
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In mares, fetal lactate uptake from the placenta increases during late gestation, although, when compared to the ovine fetus, the equine fetus appears to preferentially use glucose and lipid rather than lactate [10,11]. Hydrogen ion-dependent carriers have been found on human placental syncytiotrophoblasts both on the maternal and on the fetal side [12–14]. This system may prevent lactate from accumulating in the fetal circulation when the fetus increases its lactate production, such as during reduction in uterine blood flow and fetal hypoxia [15,16].
Amniotic fluid (AF) lactate concentration and time-dependent changes in blood lactate concentration in mares after parturition have never been evaluated. In this study, the venous blood lactate concentration of mares and foals during the first 72 h of the postpartum period was assessed, and the concentration of lactate in the AF collected during delivery and the utility of its measurement for evaluating the foal's health were investigated. This prospective observational study was carried out on mares attended at delivery. They were divided into mares delivering healthy (Group 1) and sick (Group 2) foals. The following samples were collected: AF and umbilical blood at delivery, mare's and foal's jugular blood every 12 hours from parturition until 72 h postpartum (T0-T72). Sixty-two mares were enrolled in Group 1 and 19 in Group 2. In Group 2, the survival rate was 68.4%. The median blood lactate of the foals at T0 was 3.60 mmol/L in Group 1 and 5.05 mmol/L in Group 2. The monitoring of the blood lactate concentration showed a significant time-dependent decrease from T24 in the foals (P < 0.01) and from T12 in the mares (P < 0.01). Lactate concentration over time was significantly different between healthy and sick foals (P < 0.01) but not between mares with normal and dystocic delivery (P = 0.08). A significant difference (P = 0.04) was detected as regards AF lactate concentration between Group 1 (median 14.99 mmol/L) and Group 2 (median 12.61 mmol/L). For the first time, AF lactate concentration was evaluated during parturition, and significantly higher levels were found in mares delivering healthy foals. This was an unexpected and very interesting result which warrants further investigation involving a larger number of mares. Additional studies are needed before either mare's blood or AF lactate concentration can be used in a clinical setting.
Mechanisms of Transfer Across the Human Placenta
2011, Fetal and Neonatal Physiology E-Book, Fourth Edition
Cellular Expression of the Monocarboxylate Transporter (MCT) Family in the Placenta of Mice
2010, Placenta
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Among the glucose transporter isoforms, GLUT1 and GLUT3 are localized in the cell membrane of syncytiotrophoblasts in mammals [9,10]. Another set of placental perfusion studies and isolated plasma membrane studies have demonstrated that lactate is transferred across the placental barrier by means of streospecific (between l- and d-lactate) transporters [11–13], and the movement is mediated by a carrier-dependent transporter resembling the lactate/H+ co-transporters with a broad distribution throughout the body. A representative lactate transporter is the monocarboxylate transporter (MCT) and classified SLC16 gene family.
Lactate plays an important role as an alternative energy substrate, especially in conditions with a decreased utility of glucose. Proton-coupled monocarboxylate transporters (MCTs) are essential for the transport of lactate, ketone bodies, and other monocarboxylates through the plasma membrane and may contribute to the net transport of lactate through the placental barrier. The present study examined the expression profile and subcellular localization of MCTs in the mouse placenta. An in situ hybridization survey of all MCT subtypes detected intense mRNA expressions of MCT1, MCT4, and MCT9 as well as GLUT1 in the placenta from gestational day 11.5. The expression of MCT mRNAs decreased in the intensity at the end of gestation in contrast to a consistently intense expression of GLUT1 mRNA. Immunohistochemically, MCT1 and MCT4 showed a polarized localization on the maternal side and fetal side of the two cell-layered syncytiotrophoblast, respectively. The membrane-oriented localization of MCTs was supported by the coexistence of CD147 which recruits MCT to the plasma membrane. However, the subcellular arrangement of MCT1 and MCT4 along the trophoblastic cell membrane was completely opposite of that in the human placenta. Although we cannot exactly explain the reversed localization of MCTs between human and murine placentas, it may be related to differences between humans and mice in the origin of lactate and its utilization by fetuses.
Placental transfer
2006, Knobil and Neill's Physiology of Reproduction

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Lactate carriers in the artificially perfused human term placenta

Summary

American Journal of Obstetrics and Gynecology

American Journal of Obstetrics and Gynecology

Fitting straight lines to experimental data

American Journal of Physiology

Evidence for a specific transport of d-hexoses across the human term placenta in vitro

Archiv für Gynäkologie

The permeability of capillaries in various organs as determined by use of the indicator dilution method

Acta Physiologica Scandinavica

Estimation of kinetic parameters of unidirectional transport across the blood-brain barrier

Journal of Neurochemics

Theoretical and practical significance of parallel assays of the serum lactic acid, pH and blood gases in the mothers and neonates at birth

Journal of Perinatal Medicine

An improved description of separation and performance capability of liquid scintillation counter used in dual isotope studies

Analytical Chemistry