Glucose Utilization by the Placenta and Fetal Tissues in Fed and Fasted Pregnant Rabbits

Hauguel, S.; Leturque, Armelle; Kandé, J.; Girard, Jean

doi:10.1203/00006450-198805000-00009

Cited by 15 publications

(6 citation statements)

References 31 publications

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“…Uteroplacental tissues consume 60-70 % of uterine net uptake of glucose during late pregnancy in sheep and cattle (see Bell, 1993; Table 1). Placental glucose consumption is also substantial in other species, although apparently lower in the haemochorial placenta of man (Hauguel et al 1986), rats (Leturque et al 1987), and rabbits (Hauguel et al 1988) than in the epitheliochorial placenta of ruminants. In sheep, uterine arterial glucose concentration determines the net uptake of glucose by the uterus from the maternal circulation, while changes in fetal arterial glucose concentration independently determine the partition of glucose between uteroplacental tissues and the fetus (Hay et al 1990).…”

Section: Glucose Metabolismmentioning

confidence: 96%

Regulation of placental nutrient transport and implications for fetal growth

2002

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Fetal 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.

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Section: Glucose Metabolismmentioning

confidence: 96%

Regulation of placental nutrient transport and implications for fetal growth

2002

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“…Just as in prior studies, much of the glucose entering the placenta is retained within the FPU [6,10]. Placenta is thought to have virtually no glucose-6-phosphatase activity [10,23] precluding FDG dephosphorylation.…”

Section: Discussionmentioning

confidence: 99%

“…Placenta is thought to have virtually no glucose-6-phosphatase activity [10,23] precluding FDG dephosphorylation. Recent evidence, though, suggests that glucose-6-phosphatase 3 , a more widely expressed enzyme, is expressed at midrange levels in the placenta [24].…”

Section: Discussionmentioning

confidence: 99%

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PET/CT imaging reveals unrivaled placental avidity for glucose compared to other tissues

Sawatzke¹,

Norris²,

Spyropoulos³

et al. 2015

Placenta

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Introduction The goal of this study was to define the kinetics of glucose transport from maternal blood to placenta to fetus using real time imaging. Methods Positron emission tomography (PET) imaging of the glucose tracer [18F]fluorodeoxyglucose (FDG) was used to temporally and spatially define, in vivo, the kinetics of glucose transport from maternal blood into placentae and fetuses, in the late gestational gravid rat. Computed tomography (CT), with intravenous contrast, co-registered to the PET images allowed anatomic differentiation of placentae from fetal and maternal tissues. Results FDG was rapidly taken up by placentae and subsequently appeared in fetuses with minimal temporal lag. FDG standardized uptake values in placentae and fetuses approached that of maternal brain. In both anesthetized and awake dams, one quarter of the administered FDG ultimately was accrued in the collective fetuses and placentae. Accordingly, kinetic modeling demonstrated that the placentae had very high avidity for FDG, 2-fold greater than that of the fetus and maternal brain, when accounting for the fact that fetal FDG necessarily must first be taken up by placentae. Consistent with this, placental expression of glucose transporter 1 exceeded that of all other tissues. Discussion Fetal and placental tissues place a substantial glucose metabolic burden on the mother, owing to very high avidity of placentae for glucose coupled with the large relative mass of fetal and placental tissues. Conclusions The placenta has a tremendous capacity to uptake and transport glucose. PET/CT imaging is an ideal means to study metabolite transport kinetics in the fetoplacental unit.

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“…3 Because glucose passes almost freely across the placenta, 4,5 fetal glucose levels follow those of the mother. 6 Insulin transport, in contrast, is extensively blocked by the placenta, 7 leaving fetal insulin levels much lower than maternal levels. 8,9 During periods of maternal hyperglycemia, however, the associated fetal hyperglycemia leads to secondary fetal hyperinsulinemia.…”

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confidence: 99%

Maternal Hyperglycemia Improves Fetal Cardiac Function During Tachycardia-Induced Heart Failure in Pigs

Smerup¹,

Kristiansen²,

Bøtker³

et al. 2004

Circulation

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Background-Fetal tachycardia often leads to cardiac failure, which in experimental settings can be prevented by direct fetal glucose-insulin administration. In this study, we hypothesize that similar effects can be obtained indirectly by inducing maternal hyperglycemia. Methods and Results-Systolic and diastolic indices (dP/dt max and ) of left ventricular function were measured by use of high-fidelity catheters during 180 minutes of aggressive atrial pacing (Ϸ300 bpm) in 12 preterm porcine fetuses. In 6 fetuses, maternal hyperglycemia (15 mmol/L) was induced for the last 120 minutes of pacing. The remaining fetuses served as controls. Glucose, insulin, and free fatty acid levels were determined, as was fetal myocardial glycogen content. Maternal glucose infusion led to significant fetal hyperglycemia and hyperinsulinemia but did not change the inherently low fetal levels of free fatty acids. There were no differences between groups with regard to dP/dt max (1025Ϯ226 and 1037Ϯ207 mm Hg, PϭNS) and (20.6Ϯ2.0 and 21.4Ϯ1.6 ms, PϭNS) at baseline (100%). During the 180 minutes of pacing, systolic function (dP/dt max ) and diastolic function () deteriorated more in the control group than in the hyperglycemic group (PϽ0.001 for both). At 180 minutes, dP/dt max was 62Ϯ18% of baseline in controls and 85Ϯ11% in hyperglycemic fetuses (Pϭ0.03), and was 117Ϯ12% and 98Ϯ4%, respectively (Pϭ0.004). Conclusions-Induced maternal hyperglycemia improves fetal cardiac function during fetal tachycardia and suggests a possible additional therapeutic option to improve the function of the failing fetal heart before or during antiarrhythmic therapy. The findings may be relevant in fetal heart failure in general. Key Words: heart failure Ⅲ tachycardia Ⅲ glucose D espite early diagnosis and improved therapeutic algorithms, fetal tachyarrhythmias often lead to severe cardiac failure. 1,2 Traditionally, treatment has been based on transplacental antiarrhythmic drugs, whereas little attention has been paid to metabolic support of the glucose-dependent fetal myocardium. In a porcine study, we have recently shown that direct fetal glucose-insulin infusion during tachycardia improves fetal cardiac function and metabolism. 3 Because glucose passes almost freely across the placenta, 4,5 fetal glucose levels follow those of the mother. 6 Insulin transport, in contrast, is extensively blocked by the placenta, 7 leaving fetal insulin levels much lower than maternal levels. 8,9 During periods of maternal hyperglycemia, however, the associated fetal hyperglycemia leads to secondary fetal hyperinsulinemia. 10 -14 These mechanisms suggest that induction of maternal hyperglycemia would be a possible means of generating simultaneous fetal hyperglycemia and hyperinsulinemia and thus a stimulus qualitatively similar to what we previously obtained by direct fetal glucose-insulin infusion. 3 In the present study, we test this approach as a potentially clinically relevant intervention on cardiac function and metabolism during fetal tachycardia. MethodsOne to 3 ...

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Glucose Utilization by the Placenta and Fetal Tissues in Fed and Fasted Pregnant Rabbits

Cited by 15 publications

References 31 publications

Regulation of placental nutrient transport and implications for fetal growth

Regulation of placental nutrient transport and implications for fetal growth

PET/CT imaging reveals unrivaled placental avidity for glucose compared to other tissues

Maternal Hyperglycemia Improves Fetal Cardiac Function During Tachycardia-Induced Heart Failure in Pigs

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