Fetal amino acids in normal pregnancies and in pregnancies complicated by intrauterine growth retardation

Cetin, Irene; Marconi, Anna Maria; Corbetta, Carlo; Lanfranchi, A.; Baggiani, Anna Maria; Battaglia, Frederick C.; Pardi, Giorgio

doi:10.1016/0378-3782(92)90136-5

Cited by 67 publications

(43 citation statements)

References 5 publications

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“…Similar differences between total fetal amino acids concentrations have been reported in singleton pregnancies, when IUGR and AGA fetuses were compared (20,21). These differences in amino acid profiles between MC twin pairs with different growth potentials could be a result of reduced perfusion and, thereby, transport across the placenta.…”

Section: Discussionsupporting

confidence: 52%

Discordant Amino Acid Profiles in Monochorionic Twins with Twin-Twin Transfusion Syndrome

et al. 2000

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To test the hypothesis that discordant growth in monochorionic (MC) twins occurs at least in part due to disparity in placental amino acid transporter function, we measured plasma amino acid levels by HPLC in maternal and fetal blood samples collected at birth from gestational age matched twins with (n ϭ 12) and without (n ϭ 12) twin-twin transfusion syndrome (TTTS). In the donor twin, fetal plasma concentrations and feto-maternal ratios of five essential amino acids-valine (p Ͻ 0.001), leucine (p Ͻ 0.001), iso-leucine (p Ͻ 0.05), histidine (p Ͻ 0.001) and L-arginine (p Ͻ 0.001)-were lower than the recipient and non-TTTS twin pairs. Fetal concentrations of the nonessential amino acids taurine (p Ͻ 0.001), serine (p Ͻ 0.01), glycine (p Ͻ 0.001) and tyrosine (p Ͻ 0.05) were also markedly lower in the donor than the recipient and non-TTTS twin pairs. In contrast, the fetal alanine level in the donor twin was higher than the recipient (664 Ϯ 64 versus 396 Ϯ 23 M; p Ͻ 0.001) and the non-TTTS twin pairs (p Ͻ 0.01). No such differences between amino acid profiles in non-TTTS MC twin pairs were found. Maternal plasma amino acid levels between TTTS and non-TTTS groups were comparable. This study provides the first evidence that certain amino acids in the donor twin of chronic TTTS differ significantly from those of the co-twin while others were comparable between twin pairs. These data, therefore, argue against inter-twin transfusion as the sole cause of growth restriction of the donor twin and suggests instead that impaired placental transport of amino acids may be a likely mechanism. Abbreviations MC, monochorionic F/M, feto-maternal ratio IUGR, intrauterine growth restriction TTTS, twin, twin transfusion syndrome AGA, appropriate for gestational age DC, dichorionic Perinatal death and postnatal handicap are more common in monochorionic (MC) than dichorionic (DC) twins (1). The high perinatal mortality in MC twins has been attributed to the presence of vascular anastomoses in the placenta, which may lead to twin-twin transfusion syndrome (TTTS) (2).Twin-twin transfusion syndrome is a chronic condition that presents in the early mid trimester of pregnancy, with characteristic discordance in fetal growth and amniotic fluid volume (1). Severe polyhydramnios develops in the larger "recipient" twin's sac, while oligohydramnios ensues in the growth restricted "donor" twin's sac. As pregnancy progresses, both fetuses are at a substantial risk of perinatal mortality and morbidity. The donor twin is at risk of the well described complications of severe intrauterine growth retardation, while the recipient twin may develop hydrops, cardiac dilatation, myocardial hypertrophy, tricuspid regurgitation, right ventricular outflow obstruction, and renal failure (3).Despite recent advances in the diagnostic and therapeutic modalities in fetal medicine, the treatment of chronic TTTS remains far from satisfactory (4, 5). This is attributed to the poor understanding of the patho-physiology of this enigmatic condition. Recent vascular anast...

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Section: Discussionsupporting

confidence: 52%

Discordant Amino Acid Profiles in Monochorionic Twins with Twin-Twin Transfusion Syndrome

et al. 2000

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“…The availability of techniques to sample umbilical cord blood in utero has made it possible to measure plasma amino acid concentrations prior to delivery (Daffos et al, 1985) and studies have shown that these are significantly lower in FGR compared to normal pregnancies (Cetin et al, 1990;Cetin et al, 1988;Cetin et al, 1992). Human in vivo studies with stable isotopes have shown delivery of neutral amino acids to the fetus in normal pregnancy is only just sufficient to meet requirements (Cetin, 2001), and in FGR maternofetal 13 C-leucine transfer is reduced (Marconi et al, 1999).…”

Section: Placental System a And Fetal Growth Restrictionmentioning

confidence: 99%

“…Abnormal patterns of uterine artery Doppler signal show poor sensitivity and specificity for adverse outcome (Aardema et al, 2001); this can be improved by combining Doppler with biochemical measurements of placental barrier function (Toal et al, 2008a). Furthermore, growth restricted fetuses have lower plasma concentrations of amino acids than infants of normal size (Cetin et al, 1990;Cetin et al, 1988;Cetin et al, 1992). The physicochemical characteristics of these hydrophilic nutrients dictate that they do not readily cross the placental plasma membrane, their rate of transfer is much slower than that of the gases, and is limited much more by the properties of the exchange barrier than by blood flow.…”

Section: Blood Flowmentioning

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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“…Placenta can also produce some aminoacids like glutamate and aspartate (23). Fetal amino acid concentration is usually higher than maternal levels (39). Amino acids pass through the placenta by active transport by Na+ /K+ -ATPase and H+ dependent transport.…”

Section: Fetal Protein Metabolismmentioning

confidence: 99%