Placental transport rather than maternal concentration of amino acids regulates fetal growth in monochorionic twins: Implications for fetal origin hypothesis

2001 ◽  
Vol 185 (5) ◽  
pp. 1239-1246 ◽  
Author(s):  
Rekha Bajoria ◽  
Suren R. Sooranna ◽  
Stuart Ward ◽  
Stephen D’Souza ◽  
Maggie Hancock
Keyword(s):  
Amino Acids ◽  
Fetal Growth ◽  
Monochorionic Twins ◽  
Placental Transport ◽  
Fetal Origin ◽  
Origin Hypothesis

scholarly journals Regulation of placental nutrient transport and implications for fetal growth

2002 ◽  
Vol 15 (2) ◽  
pp. 211-230 ◽  
Author(s):  
Alan W Bell ◽  
Richard A Ehrhardt
Keyword(s):  
Amino Acids ◽  
Fetal Growth ◽  
Maternal Nutrition ◽  
Nutrient Transport ◽  
Late Pregnancy ◽  
Late Gestation ◽  
Abnormal Development ◽  
Placental Transport ◽  
Specific Transport

AbstractFetal macronutrient requirements for oxidative metabolism and growth are met by placental transport of glucose, amino acids, and, to a lesser extent that varies with species, fatty acids. It is becoming possible to relate the maternal–fetal transport kinetics of these molecules in vivo to the expression and distribution of specific transporters among placental cell types and subcellular membrane fractions. This is most true for glucose transport, although apparent inconsistencies among data on the roles and relative importance of the predominant placenta glucose transporters, GLUT-1 and GLUT-3, remain to be resolved. The quantity of macronutrients transferred to the fetus from the maternal bloodstream is greatly influenced by placental metabolism, which results in net consumption of large amounts of glucose and, to a lesser extent, amino acids. The pattern of fetal nutrient supply is also altered considerably by placental conversion of glucose to lactate and, in some species, fructose, and extensive transamination of amino acids. Placental capacity for transport of glucose and amino acids increases with fetal demand as gestation advances through expansion of the exchange surface area and increased expression of specific transport molecules. In late pregnancy, transport capacity is closely related to placental size and can be modified by maternal nutrition. Preliminary evidence suggests that placental expression and function of specific transport proteins are influenced by extracellular concentrations of nutrients and endocrine factors, but, in general, the humoral regulation of placental capacity for nutrient transport is poorly understood. Consequences of normal and abnormal development of placental transport functions for fetal growth, especially during late gestation, and, possibly, for fetal programming of postnatal disorders, are discussed.

scholarly journals Placental transport in response to altered maternal nutrition

2012 ◽  
Vol 4 (2) ◽  
pp. 101-115 ◽  
Author(s):  
F. Gaccioli ◽  
S. Lager ◽  
T. L. Powell ◽  
T. Jansson
Keyword(s):  
Amino Acids ◽  
Blood Flow ◽  
Fetal Growth ◽  
Maternal Nutrition ◽  
Critical Role ◽  
Placental Function ◽  
Maternal Undernutrition ◽  
Placental Transport ◽  
Placental Blood ◽  
Placental Blood Flow

The mechanisms linking maternal nutrition to fetal growth and programming of adult disease remain to be fully established. We review data on changes in placental transport in response to altered maternal nutrition, including compromized utero-placental blood flow. In human intrauterine growth restriction and in most animal models involving maternal undernutrition or restricted placental blood flow, the activity of placental transporters, in particular for amino acids, is decreased in late pregnancy. The effect of maternal overnutrition on placental transport remains largely unexplored. However, some, but not all, studies in women with diabetes giving birth to large babies indicate an upregulation of placental transporters for amino acids, glucose and fatty acids. These data support the concept that the placenta responds to maternal nutritional cues by altering placental function to match fetal growth to the ability of the maternal supply line to allocate resources to the fetus. On the other hand, some findings in humans and mice suggest that placental transporters are regulated in response to fetal demand signals. These observations are consistent with the idea that fetal signals regulate placental function to compensate for changes in nutrient availability. We propose that the placenta integrates maternal and fetal nutritional cues with information from intrinsic nutrient sensors. Together, these signals regulate placental growth and nutrient transport to balance fetal demand with the ability of the mother to support pregnancy. Thus, the placenta plays a critical role in modulating maternal–fetal resource allocation, thereby affecting fetal growth and the long-term health of the offspring.

scholarly journals Regulation of Nutrient Transport across the Placenta

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Susanne Lager ◽  
Theresa L. Powell
Keyword(s):  
Cardiovascular Disease ◽  
Amino Acids ◽  
Fetal Growth ◽  
Nutrient Transport ◽  
Intervention Strategies ◽  
Regulatory Mechanisms ◽  
Nutrient Transporters ◽  
Perinatal Complications ◽  
Placental Transport ◽  
Increased Risk

Abnormal fetal growth, both growth restriction and overgrowth, is associated with perinatal complications and an increased risk of metabolic and cardiovascular disease later in life. Fetal growth is dependent on nutrient availability, which in turn is related to the capacity of the placenta to transport these nutrients. The activity of a range of nutrient transporters has been reported to be decreased in placentas of growth restricted fetuses, whereas at least some studies indicate that placental nutrient transport is upregulated in fetal overgrowth. These findings suggest that changes in placental nutrient transport may directly contribute to the development of abnormal fetal growth. Detailed information on the mechanisms by which placental nutrient transporters are regulated will therefore help us to better understand how important pregnancy complications develop and may provide a foundation for designing novel intervention strategies. In this paper we will focus on recent studies of regulatory mechanisms that modulate placental transport of amino acids, fatty acids, and glucose.

DIAGNOSIS AND MANAGEMENT OF SELECTIVE FETAL GROWTH RESTRICTION IN MONOCHORIONIC TWINS

2009 ◽  
Vol 20 (4) ◽  
pp. 269-281 ◽  
Author(s):  
EDUARD GRATACÓS ◽  
ELISENDA EIXARCH ◽  
FATIMA CRISPI
Keyword(s):  
Fetal Growth ◽  
Common Sense ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Fetal Weight ◽  
Abdominal Circumference ◽  
Monochorionic Twins ◽  
Normal Ranges ◽  
Estimated Fetal Weight ◽  
Simple Definition

Selective fetal growth restriction (sFGR) has been reported to occur in about 10–15% of monochorionic (MC) twins. The diagnosis of sFGR has been based on variable criteria including estimated fetal weight (EFW), abdominal circumference and/or the degree of fetal weight discordance. Recent studies tend to use a simple definition which includes the presence of an EFW less than the 10th percentile in the smaller twin. Some would argue that the intertwin fetal weight discordance should be included in the definition. Indeed this factor plays a major role in the complications presented by these cases. While the majority of cases with one fetus below the 10th percentile usually will also present with a large intertwin EFW discordance, the contrary is not always true. Thus, it is possible to find MC twins with remarkable intertwin EFW discordance but the EFW of both fetuses are still within normal ranges. Although it appears to be common sense that a large intertwin discrepancy might represent a higher risk for some of the complications described later in this review, there is no consistent evidence to support this notion. Therefore, due to its simplicity, a definition based on an EFW below 10th percentile in one twin is probably the most useful for clinical and research purposes.

scholarly journals Effects of maternal iron restriction in the rat on hypoxia-induced gene expression and fetal metabolite levels

2001 ◽  
Vol 85 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Rohan M. Lewis ◽  
Lynwen A. James ◽  
Junlong Zhang ◽  
Christopher D. Byrne ◽  
C. Nicholas Hales
Keyword(s):  
Amino Acids ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Plasma Levels ◽  
Plasma Cholesterol ◽  
Maternal Plasma ◽  
Fetal Growth Retardation ◽  
Restricted Diet ◽  
Fetal Plasma ◽  
Restricted Group

The mechanism by which maternal Fe deficiency in the rat causes fetal growth retardation has not been clearly established. This study compared the effects on the fetuses from dams fed a control diet with two groups of dams fed Fe-restricted diets. One Fe-restricted group was fed the Fe-restricted diet for 1 week prior to mating and throughout gestation and the second Fe-restricted group was fed the Fe-restricted diet for 2 weeks prior to mating and throughout gestation. On day 21 of gestation Fe-restricted dams, and their fetuses, were anaemic. Fetal weight was reduced in both Fe-restricted groups compared with controls. Expression of hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) are induced by hypoxia. The levels of HIF-1α mRNA were highest in placenta, then in kidney, heart and liver but were not different between the groups. Levels of plasma VEGF were not different between the groups. Maternal plasma triacylglycerol was decreased in the 1-week Fe-restricted dams compared with controls. Maternal plasma cholesterol and free fatty acid levels were not different between the groups. In fetal plasma, levels of triacylglycerol and cholesterol were decreased in both Fe-restricted groups. In maternal plasma, levels of a number of amino acids were elevated in both Fe-restricted groups. In contrast, levels of a number of amino acids in fetal plasma were lower in both Fe-restricted groups. Fetal plasma lactate was increased in Fe-restricted fetuses but fetal plasma glucose and β-hydroxybutyrate were not affected. These changes in fetal metabolism may contribute to fetal growth retardation in this model. This study does not support the hypothesis that the Fe-restricted fetus is hypoxic.

Placental Transport of Model Amino Acids.

1962 ◽  
Vol 109 (3) ◽  
pp. 700-702 ◽  
Author(s):  
B. H. Feldman ◽  
H. N. Christensen
Keyword(s):  
Amino Acids ◽  
Placental Transport

Dietary rumen-protected arginine and N-carbamylglutamate supplementation enhances fetal growth in underfed ewes

2018 ◽  
Vol 30 (8) ◽  
pp. 1116 ◽  
Author(s):  
Lingwei Sun ◽  
Hao Zhang ◽  
Ziyu Wang ◽  
Yixuan Fan ◽  
Yixuan Guo ◽  
...  
Keyword(s):  
Amino Acids ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Plasma Concentrations ◽  
Longissimus Dorsi ◽  
Somatotropic Axis ◽  
Longissimus Dorsi Muscle ◽  
Fetal Plasma ◽  
Dorsi Muscle ◽  
Pregnant Sheep

The present study was conducted with an ovine intrauterine growth restriction (IUGR) model to test the hypothesis that dietary rumen-protected l-arginine (RP-Arg) or N-carbamylglutamate (NCG) supplementation in underfed ewes is effective in enhancing fetal growth. Between Days 35 and 110 of pregnancy, 32 multiparous ewes carrying two fetuses were randomly assigned to one of four groups: a control (CG) group (n = 8; 100% National Research Council (NRC) requirements for pregnant sheep), a nutrient-restricted (RG) group (n = 8; fed 50% NRC requirements, and two treatment (ARG and NCG) groups (n = 8 in each group; fed 50% NRC requirements supplemented with 20 g day−1 RP-Arg or 5 g day−1 NCG. All ewes were killed on Day 110 of pregnancy to determine fetal weight and fetal organ weights, and metabolites and hormones in fetal plasma, amino acid concentrations in the fetal liver and longissimus dorsi muscle, and expression of mRNAs in the somatotropic axis. Maternal and fetal bodyweight and the weight of most fetal organs expressed as a percentage of bodyweight increased in response to ARG and NCG compared with values for fetuses from RG ewes. Fetal plasma concentrations of insulin, insulin-like growth factor 1, total amino acids, lactate, thyroxine, and the thyroxine/tri-iodothyronine ratio were lower in fetuses from RG ewes compared with the other treatment groups, but concentrations of growth hormone, non-esterified fatty acids, and total cholesterol were greater in fetuses from RG ewes. Maternal RP-Arg or NCG supplementation increased concentrations of amino acids in fetal tissues and expression of mRNAs for somatotropic axis proteins in fetuses from RG ewes. These findings suggest that maternal RP-Arg and NCG supplementation of underfed ewes decreases fetal IUGR by improving metabolic homeostasis of fetal endocrinology, increasing the availability of amino acids in the fetal liver and longissimus dorsi muscle and affecting the expression of somatotropic axis genes.

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