Model of placental glucose consumption and glucose transfer

Hay, William W.; Molina, Rafael; DiGiacomo, J. E.; Meschia, Giacomo

doi:10.1152/ajpregu.1990.258.3.r569

Cited by 51 publications

(65 citation statements)

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“…The control data for hepatic and umbilical uptakes are in good agreement with previous measurements (3,5,8,12,13,18,23,25). However, this is the first study in which the fetal hepatic uptakes of glucose and all major glucogenic substrates have been measured in the same experimental preparation.…”

Section: Discussionsupporting

confidence: 88%

“…The transport rate of maternal glucose to the fetus is a function of the glucose concentration difference between maternal and fetal plasma (12). We surmise that fetal hepatic glucose production was the main cause of the increase in fetal plasma glucose, which in turn caused a decrease in the transplacental glucose concentration gradient that drives maternal glucose into the umbilical circulation.…”

Section: Discussionmentioning

confidence: 91%

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Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Teng

Battaglia

Meschia

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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Wilkening. Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion. Am J Physiol Endocrinol Metab 282: E542-E550, 2002; 10.1152/ajpendo.00248.2001.-To test the hypothesis that fetal hepatic glutamate output diverts the products of hepatic amino acid metabolism from hepatic gluconeogenesis, ovine fetal hepatic and umbilical uptakes of glucose and glucogenic substrates were measured before and during fetal glucagonsomatostatin (GS) infusion and during the combined infusion of GS, alanine, glutamine, and arginine. Before the infusions, hepatic uptake of lactate, alanine, glutamine, arginine, and other substrates was accompanied by hepatic output of pyruvate, aspartate, serine, glutamate, and ornithine. The GS infusion induced hepatic output of 1.00 Ϯ 0.07 mol glucose carbon/mol O 2 uptake, an equivalent reduction in hepatic output of pyruvate and glutamate carbon, a decrease in umbilical glucose uptake and placental uptake of fetal glutamate, an increase in hepatic alanine and arginine clearances, and a decrease in umbilical alanine, glutamine, and arginine uptakes. The latter result suggests that glucagon inhibits umbilical amino acid uptake. We conclude that fetal hepatic pyruvate and glutamate output is part of an adaptation to placental function that requires the fetal liver to maintain both a high rate of catabolism of glucogenic substrates and a low rate of gluconeogenesis. fetal liver; placenta; glutamate; fetal gluconeogenesis UNDER NORMAL PHYSIOLOGICAL CONDITIONS, the liver of the ovine fetus releases glutamate in the fetal circulation (18,23,25). About one-third of the glutamate released is produced from hydrolysis of plasma glutamine (25), and the remainder is produced via hepatic oxidative metabolism. The fetal infusion of uniformly labeled [ 13 C]lactate results in the appearance of hepatic venous glutamate, which is labeled mostly with either one or two 13

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 91%

Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Teng

Battaglia

Meschia

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…Which of these several factors led to the small increase in fetal plasma arginine enrichment in period 2 cannot be determined from the data in this study. Confirmation of these observations will require a more complete experimental approach with bidirectional kinetic analysis of tracers and tracee infused into the mother and the fetus at different maternal and fetal arginine concentrations, similar to our previously published kinetic analysis of placental glucose transfer and metabolism (23).…”

supporting

confidence: 55%

Ovine Placental and Fetal Arginine Metabolism at Normal and Increased Maternal Plasma Arginine Concentrations

et al. 2002

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Arginine (A) may play a significant role in fetal growth, by stimulating insulin secretion and as a precursor for both polyamine synthesis and nitric oxide production. To determine whether increased maternal plasma A concentrations can enhance delivery of A to the fetus, uterine, umbilical, and net uteroplacental (UP) A uptake rates were measured in 12 pregnant ewes at 129.6 Ϯ 0.4 d gestation (mean Ϯ SEM) during normal and after 3 h of increased maternal plasma A concentrations. With a 2.7-fold increase in maternal plasma A concentrations (p Ͻ 0.001), there were significant increases in uterine A uptake (13.8 Ϯ 1.0 to 41.3 Ϯ 7.7 mol/min, p Ͻ 0.005), umbilical A uptake (3.3 Ϯ 0.5 to 5.2 Ϯ 0.8 mol·min Ϫ1 ·kg Ϫ1 fetus, p Ͻ 0.005), UP A uptake (17.8 Ϯ 6.2 to 89.2 Ϯ 20.3 mol·min Ϫ1 ·kg Ϫ1 placenta, p Ͻ 0.01), fetal arterial A concentration (98.7 Ϯ 6.3 to 137.1 Ϯ 9.9 M, p Ͻ 0.001), maternal A disposal rate (143.7 Ϯ 9.4 to 217.0 Ϯ 6.7 mol/min, p Ͻ 0.001), fetal A disposal rate (7.9 Ϯ 0.8 to 9.9 Ϯ 1.1 mol·min Ϫ1 ·kg Ϫ1 , p Ͻ 0.05), fetal A oxidation rate (1.31 Ϯ 0.24 to 1.84 Ϯ 0.36 mol·min Ϫ1 ·kg Ϫ1 , p Ͻ 0.05), and plasma insulin concentration in both fetus (16 Ϯ 2 to 20 Ϯ 2 U/mL, p Ͻ 0.001) and mother (24 Ϯ 3 to 32 Ϯ 4 U/mL, p Ͻ 0.001). Thus, increased maternal plasma A concentration increases maternal, UP, and fetal A net uptake, and increases insulin secretion in mother and fetus. The 4.2-fold larger increase in UP than net fetal A uptake could represent preferential UP A metabolism relative to fetal A metabolism, relatively limited placental-fetal A transport capacity compared with uterine A uptake capacity, or both; responsible mechanisms remain unknown. Arginine is a conditionally indispensable amino acid in the mammalian fetus and neonate (1, 2), and maintenance of fetal arginine supply and plasma concentrations are important for optimal fetal growth. The mechanisms by which arginine promotes fetal growth, however, are multifaceted and have not been adequately investigated. Arginine is an insulin secretagogue in ovine and human fetuses (3-7) and in human newborns (8 -10); thus the role of arginine in fetal growth may include an insulin-mediated anabolic effect. In addition, arginine could stimulate growth as a precursor for polyamine synthesis (11) and nitric oxide production (12-14).In contrast, arginine deficiency has been shown to induce growth restriction in experimental animals (15, 16). A potential therapy for fetal growth restriction, therefore, could include maternal plasma arginine supplementation in an attempt to increase fetal arginine supply. It is not known, however, whether increasing maternal plasma arginine concentration could increase net fetal arginine uptake, fetal plasma arginine concentration, or fetal insulin concentration. In addition, the characteristics of placental arginine uptake, metabolism, and transport to the fetus have not been determined. Therefore, this study was designed to determine how maternal arginine supplementation affects maternal, uteroplacental, and fetal arginine net ...

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“…The human placental perfusion studies demonstrate that the maternal to fetal glucose gradient is a major determinant of fetal blood glucose concentrations and may be based on polarized glucose transporter concentration differences in the trophoblast. Data from in vivo sheep studies by Hay et al have also shown that the maternal to fetal glucose gradient is the major driving force for fetal glucose concentration [95]. It has also been determined in both sheep and humans that the transplacental glucose gradient is increased near term as a result of decreasing fetal glucose concentrations [96,97].…”

Section: Placental Glucose Transfer and Metabolismmentioning

confidence: 95%

The pregnant sheep as a model for human pregnancy

2008

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Successful outcome of human pregnancy not only impacts the quality of infant life and well-being, but considerable evidence now suggests that what happens during fetal development may well impact health and well-being into adulthood. Consequently, a thorough understanding of the developmental events that occur between conception and delivery is needed. For obvious ethical reasons, many of the questions remaining about the progression of human pregnancy can not be answered directly, necessitating the use of appropriate animal models. A variety of animal models exist for the study of both normal and compromised pregnancies, including laboratory rodents, non-human primates and domestic ruminants. While all of these animal models have merit, most suffer from the inability to repetitively sample from both the maternal and fetal side of the placenta, limiting their usefulness in the study of placental or fetal physiology under non-stressed in vivo conditions. No animal model truly recapitulates human pregnancy, yet the pregnant sheep has been used extensively to investigate maternal-fetal interactions. This is due in part to the ability to surgically place and maintain catheters in both the maternal and fetal vasculature, allowing repeated sampling from non-anesthetized pregnancies. Considerable insight has been gained on placental oxygen and nutrient transfer and utilization from use of pregnant sheep. These findings were often confirmed in human pregnancies once appropriate technologies became available. The purpose of this review is to provide an overview of human and sheep pregnancy, with emphasis placed on placental development and function as an organ of nutrient transfer.

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Model of placental glucose consumption and glucose transfer

Cited by 51 publications

References 0 publications

Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Fetal hepatic and umbilical uptakes of glucogenic substrates during a glucagon-somatostatin infusion

Ovine Placental and Fetal Arginine Metabolism at Normal and Increased Maternal Plasma Arginine Concentrations

The pregnant sheep as a model for human pregnancy

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