Placental Transport and Metabolism of Amino Acids

Battaglia, Frederick C.; Regnault, Timothy R. H.

doi:10.1053/plac.2000.0612

Cited by 151 publications

(101 citation statements)

References 120 publications

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“…Least square means with different letter superscripts depict differences (P < 0.05). Discussions on uteroplacental and fetal uptake of AA can be primarily divided into two areas of interest focusing on either metabolic pathways or transport systems (Battaglia and Regnault, 2001;Jansson, 2001;Fowden et al, 2006). From a metabolic standpoint, previous research has shown consistent uterine and fetal uptakes of essential AA (Chung et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…This increased fetal uptake cannot be entirely dependent upon maternal blood concentrations of BCAA, which were not different in maternal artery or gravid uterine vein. Therefore, placental nutrient transport capacity of BCAA, accomplished primarily via sodium independent transporter system I (Battaglia and Regnault, 2001;Jansson, 2001), may be decreased during maternal nutrient restriction and rescued by melatonin supplementation. This would account for the dramatic differences in maternal and fetal concentrations of BCAA across our treatment groups.…”

Section: Discussionmentioning

confidence: 99%

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Dietary melatonin supplementation alters uteroplacental amino acid flux during intrauterine growth restriction in ewes

Lemley

Camacho

Meyer

et al. 2013

Animal

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Dietary melatonin supplementation during mid-to late-gestation increased umbilical artery blood flow and caused disproportionate fetal growth. This melatonin-induced increase in umbilical artery blood flow may alter nutrient availability to the fetus, which may lead to alterations in fetal size. The objectives of the current experiment were to determine amino acid (AA) and glucose concentrations as well as AA and glucose flux across the uteroplacenta using a mid-to late-gestation model of intrauterine growth restriction supplemented with dietary melatonin as a 2 3 2 factorial design. At day 50 of gestation, 32 ewes were supplemented with 5 mg of melatonin (MEL) or no melatonin (CON) and were allocated to receive 100% (adequate; ADQ) or 60% (restricted; RES) of nutrient requirements. On day 130 of gestation, uterine and umbilical blood flows were determined via Doppler ultrasonography during a non-survival surgery. Blood samples were collected under general anesthesia from the maternal saphenous artery, gravid uterine vein, umbilical artery, and umbilical vein for AA analysis and glucose. Total a-AA concentrations in maternal artery and gravid uterine vein were decreased (P , 0.05) in RES v. ADQ fed ewes. Maternal arterial 2 venous difference in total a-AA was increased ( P < 0.01) in RES v. ADQ fed ewes, while total uterine a-AA flux was not different (P . 0.40) across all treatment groups. Fetal venous 2 arterial difference in total a-AA as well as uteroplacental flux of total a-AA were decreased (P , 0.05) in CON-RES v. CON-ADQ, and similar (P . 0.20) in MEL-RES v. CON-ADQ. Maternal concentrations and uterine flux of branched-chain AA (BCAA) were not different across all treatment groups; however, fetal uptake of BCAA was decreased (P , 0.05) in CON-RES v. CON-ADQ, and similar (P . 0.20) in MEL-RES v. CON-ADQ. Uterine uptake of glucose was not different (P > 0.08) across all treatment groups, while uteroplacental uptake of glucose was increased (P < 0.05) in RES v. ADQ ewes. In conclusion, maternal nutrient restriction increased maternal arterial 2 venous difference in total a-AA, while total uterine a-AA flux was unaffected by maternal nutrient restriction. Melatonin supplementation did not impact maternal serum concentrations or uterine flux of glucose or AA; however, melatonin did improve fetal BCAA uptake during maternal nutrient restriction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dietary melatonin supplementation alters uteroplacental amino acid flux during intrauterine growth restriction in ewes

Lemley

Camacho

Meyer

et al. 2013

Animal

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“…Analysis of the different amino acid transporters found in the placenta has been challenging due to the large number of amino acid substrates, the overlapping specificity of the transporters, and the complicating factor of placental metabolism and utilisation of amino acids (Battaglia, 1986). Based on competitive interactions between amino acid substrates, at least 15 transport systems for neutral, basic and acidic amino acids have been identified in the placenta analogous to those described for other epithelia (Jansson, 2001;Moe, 1995).…”

Section: Amino Acid Transportmentioning

confidence: 99%

Placental nutrient supply and fetal growth

Desforges¹,

Sibley²

2010

Int. J. Dev. Biol.

147

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This review considers mechanisms by which transfer across the placenta takes place and how the capacity of the placenta to supply nutrients relates to fetal growth and vice versa. Blood flow through both uterine and umbilical circulations of the placenta, the structural properties of the placental exchange barrier and its related diffusional permeability, and the expression and activity of a wide range of transporter proteins in the syncytiotrophoblast, the transporting epithelium of the placenta, all need to be taken into account in considering placental supply capacity. We discuss the evidence that each of these factors affects, and is affected by, fetal growth rate and consider the regulatory mechanisms involved, with a particular focus on data that has emerged from study of the system A amino acid transporter. We consider that future work will build on the considerable foundation of knowledge regarding placental transfer mechanisms, as well as the other aspects of placental structure and function, to develop new diagnostic and therapeutic strategies for pregnancy complications, such as fetal growth restriction or overgrowth.

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“…Both branched chain amino acids and phenylalanine have been shown to use this exchange transporter' (Battaglia and Regnault, 2001). Sturtevant (1985) (abstract): 'Phenylalanine is concentrated on the foetal side of the placenta'.…”

Section: Box 1 Continued Comments Of Jd Fernstrommentioning

confidence: 99%

Addressing comments by JD Fernstrom

Humphries

Pretorius

2008

Eur J Clin Nutr

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The issue of aspartame safety has been controversial since approval by FDA, many years ago. It seems as if there are two points of views, either supporting the use of aspartame, or suggesting its dangers. Numerous research articles raised concerns regarding the adverse effects and particularly related to the metabolic components. The comments of JD Fernstrom will now be addressed in Box 1.From the comments made by JD Fernstrom, it appears that he does not trust research suggesting that aspartame may be detrimental to human health. We believe that there are numerous well-researched papers by key researchers that prove the negative effects of this sweetener. Can we as researchers really take the responsibility of the health of millions of consumers by ignoring research? Can we sit back ), and we acknowledge the fact that there are articles that propagate the fact that aspartame is safe, it was the focus of the article to discuss possible adverse effects of the consumption of aspartame. Formate is not converted to diketopiperazine (abstract) Sentence in the abstract of Humphries et al. (2007) is as follows: methanol, which forms 10% of the broken down product, is converted in the body to formate, which can either be excreted or can give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives. This sentence does not imply that formate is converted to diketopiperazine, but that diketopiperazine is a breakdown product of methanol. (Prodolliet and Bruelhart, 1993;Lin and Cheng, 2000). The authors are incorrect in stating that tyrosine cannot be synthesized in brain from phenylalanine. This statement is not true; under the heading 'Effects of phenylalanine', the sentence reads 'A large number of compounds, including phenylalanine and tyrosine compete with each other for a binding site on the NAAT, seeing that it is the only manner in which these compounds can cross the BBB. Importantly, tyrosine cannot be synthesised in the brain, thus have to enter the BBB via NAAT (Figure 2c) for production'. For more clarity, the sentence could also have read 'Importantly, dopamine cannot be synthesized in the brain unless tyrosine is carried over the BBB via NAAT for production'. Despite the authors' statement, even very large increases in phenylalanine levels produced by aspartame administration to rats do not suppress catecholamine synthesis rate (Dow-Edwards et al., 1989) Reference: There are papers that disagree with the statement of JD Fernstrom: Yokogoshi and Wurtman (1986), which states 'Phenylalanine has been described as both a substrate (Kaufman S, personal communication) and an inhibitor (McKean, 1972;Gibson and Wurtman, 1977) of tyrosine hydroxylase, the enzyme that catalyzes the rate-limiting step in converting tyrosine to catecholamines'. 'The effect of TPT (tryptophan, phenylalanine and tyrosine) depletion on the ratio between the monoamine precursors and other LNAA that compete for active transport into the brain correspond to an 87-90% decrease. Neuro-imaging, cerebro...

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Placental Transport and Metabolism of Amino Acids

Cited by 151 publications

References 120 publications

Dietary melatonin supplementation alters uteroplacental amino acid flux during intrauterine growth restriction in ewes

Dietary melatonin supplementation alters uteroplacental amino acid flux during intrauterine growth restriction in ewes

Placental nutrient supply and fetal growth

Addressing comments by JD Fernstrom

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