Maternal-fetal glucose exchange: necessity of a three-pool model

1984 ◽  
Vol 246 (6) ◽  
pp. E528-E534 ◽  
Author(s):  
W. W. Hay ◽  
J. W. Sparks ◽  
F. C. Battaglia ◽  
G. Meschia
Keyword(s):  
Glucose Utilization ◽  
Maternal Blood ◽  
Fetal Blood ◽  
Entry And Exit ◽  
Tissue Mass ◽  
Pregnant Uterus ◽  
Fick Principle ◽  
Pregnant Sheep ◽  
Pool Model ◽  
Net Flux

Tracer glucose was infused simultaneously into mother ( [6-3H]glucose) and fetus ( [U-14C]glucose) in pregnant sheep in the last month of gestation to study the exchange of glucose molecules between maternal and fetal blood. Net rates of entry and exit of tracer glucose via the uterine and umbilical circulations were measured by application of the Fick principle under steady-state conditions. The net flux of fetal tracer to the uteroplacenta from the fetus was 53.4 +/- 3.1% of the fetal tracer infusion. The net flux of fetal tracer into maternal blood was 43.8 +/- 5.0% of the net flux of fetal tracer to the uteroplacenta from fetal blood. The net flux of maternal tracer to the uterus from the mother was 31.7 +/- 2.8% of the maternal tracer infusion. The net flux of maternal tracer into fetal blood was 40.5 +/- 4.4% of the net flux to pregnant uterus from maternal blood. This evidence demonstrates that the uteroplacental tissue mass constitutes a glucose pool that is interposed between the maternal and fetal glucose pools and rapidly metabolizes glucose molecules derived from both maternal and fetal blood. Calculations based on a three-pool model show that the fetal glucose pool contributes approximately 40% of the glucose that is metabolized by the placenta. The comparison of the three-pool model with a previously proposed two-pool reversible model shows that the latter lumps the placental utilization of fetal glucose with fetal glucose utilization and overestimates the rate of fetal glucose metabolism by approximately 60%.

Uterine blood flow and oxygen consumption in pregnant sheep and goats

1959 ◽  
Vol 197 (4) ◽  
pp. 929-934 ◽  
Author(s):  
James Metcalfe ◽  
Seymour L. Romney ◽  
Joseph R. Swartwout ◽  
Donald M. Pitcairn ◽  
Anton N. Lethin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Nitrous Oxide ◽  
Oxygen Consumption ◽  
Maternal Blood ◽  
Uterine Blood Flow ◽  
Human Beings ◽  
Pregnant Uterus ◽  
Fick Principle ◽  
Pregnant Sheep ◽  
Made In

This report deals with the volume of maternal blood flow to the pregnant uterus of the sheep and goat. Studies were made in 2 nonpregnant animals and in 20 pregnant animals at known stages of gestation. Measurements of uterine blood flow were made using nitrous oxide according to the Fick principle. The results indicate that in the nonpregnant uterus the blood flow is approximately 25 ml/min. It increases to approximately 200 ml/min. at the 80th day of gestation and exceeds 1000 ml/min. near the end of the 150-day gestation period of these animals. Data are also included for calculation of uterine O2 consumption. The findings with regard to uterine blood flow and O2 consumption are discussed in relation to previous findings in human beings and in rabbits.

Effects of fetal insulin infusion on glucose kinetics in pregnant sheep: a compartmental analysis

1986 ◽  
Vol 251 (4) ◽  
pp. E448-E456 ◽  
Author(s):  
C. A. Bloch ◽  
W. Banach ◽  
K. Landt ◽  
S. Devaskar ◽  
M. A. Sperling
Keyword(s):  
Glucose Uptake ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Compartmental Analysis ◽  
Compartment Model ◽  
Base Line ◽  
Glucose Kinetics ◽  
Fick Principle ◽  
Pregnant Sheep

A three-compartment model, consisting of fetus (F), uteroplacenta, and mother (M) was applied to quantitate the effects of fetal hyperinsulinemia on glucose kinetics in pregnant sheep late in gestation. The approach combines the Fick principle with isotope dilution of differentially labeled glucose isotopes, infused simultaneously to F [U-14C]- and M [2-3H]glucose. In the basal state, rates of umbilical glucose uptake (8.37 +/- 0.98 mg/kg per min) and fetal glucose utilization (7.38 +/- 1.13) were equivalent (mean +/- SE; n = 12). When fetal insulin was increased from 13.7 +/- 2.2 to a plateau of approximately 100 microU/ml, arterial glucose decreased from 18.9 +/- 0.8 to a new steady state of approximately 13 mg/dl (P less than 0.001). Whereas umbilical glucose uptake increased at 90 min and remained elevated thereafter (P less than 0.01), fetal glucose utilization increased only transiently at 60 min by 1.9 +/- 0.8 mg/kg per min (26%; P less than 0.05) and then returned to base line. Insulin's persistent effect, however, was evident from the sustained doubling of the glucose clearance rate from 39.3 +/- 5.9 to 66.6 +/- 10.5 ml/kg per min (P less than 0.005). No endogenous fetal glucose production was evident throughout the experiments. Maternal glucose production and utilization remained unchanged, although there was a small decline in M glucose concentration and an increase in glucose transfer from M to the uteroplacenta and F, from 33.9 +/- 8.1 to 48.1 +/- 7.0 mg/min at 60 min (P less than 0.01 by paired analysis). We conclude that fetal hyperinsulinemia initially lowers glucose concentration by transiently increasing fetal glucose utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative aspects of glucose metabolism in pregnant and nonpregnant sheep

1963 ◽  
Vol 204 (1) ◽  
pp. 147-152 ◽  
Author(s):  
E. N. Bergman
Keyword(s):  
Glucose Oxidation ◽  
Glucose Utilization ◽  
The Body ◽  
Glucose Turnover ◽  
Turnover Rates ◽  
Pregnant Sheep ◽  
The Mean ◽  
Total Glucose ◽  
Mean Glucose ◽  
Pool Sizes

Labeled glucose was infused into four groups of ewes: nonpregnant fed; nonpregnant fasted; twin-pregnant fed; and twin-pregnant hypoglycemic and ketonemic. Mean glucose pool sizes were 157 and 127 mg/kg in nonpregnant and pregnant ewes, respectively, with decreased values in both fasting and hypoglycemia. Nonpregnant animals had glucose turnover rates averaging 4.0 g/hr (0.22 g/hr·kg3/4) when fed and only 2.7 g/hr (0.15 g/hr·kg3/4) after fasting. These values were only 60–80% of that of pregnant sheep, implying that glucose utilization due to twin-pregnancy was 20–40% of the total. The mean glucose space was about 27% of the body weight, indicating predominantly extracellular distribution of glucose even in hypoglycemia. In all animals about 8–10% of the exhaled CO2 was found to be derived from glucose oxidation and about one-third of the total glucose turnover was used for CO2 production. Comparisons of these data to values obtained from other mammals indicated further that there is a lower rate of glucose oxidation and metabolism in ruminants.

Oxygen equilibrium properties of blood and hemoglobin of fetal and adult Weddell seals

1981 ◽  
Vol 50 (5) ◽  
pp. 999-1005 ◽  
Author(s):  
J. Qvist ◽  
R. E. Weber ◽  
W. M. Zapol
Keyword(s):  
Whole Blood ◽  
Maternal Blood ◽  
Bohr Effect ◽  
Red Cell ◽  
Fetal Blood ◽  
Maternal Circulation ◽  
Weddell Seals ◽  
Blood Ph ◽  
Ph Decrease ◽  
2,3 Dpg

Oxygen equilibria of whole blood and hemoglobins from adult and fetal Weddell seals are reported. The maternal blood shows a lower O2 affinity than the fetal blood (halfsaturation O2 tension P50 = 26.9 +/- 1.18 and 21.4 +/- 1.25 Torr, respectively, at 37 degrees C and pH 7.4), and a greater Bohr effect (delta log P50/delta pH = -0.49 and -0.31, respectively, at pH 7.4-6.8), correlated with higher red cell 2,3-diphosphoglycerate (2,3-diphosphoglycerate (2,3-DPG) concentrations (6.45 +/- 0.81 mmol.1-1, compared to 2.65 +/- 0-42 mmol.1-1 in the fetus). Both the maternal and fetal erythrocytes contain two major and two minor hemoglobin components occurring in the same ratio and the 2,3-DPG-free whole hemolysates, as well as the isolated major components from each stage, show the same oxygenation properties, ascribing the whole-blood differences to the higher adult DPG levels. A 2,3-DPG effect also appears to account for the disparity in the Bohr effects, which will favor unloading of O2 from the maternal circulation during diving as maternal and fetal blood pH decrease in parallel.

scholarly journals Maternal inflammation at midgestation impairs subsequent fetal myoblast function and skeletal muscle growth in rats, resulting in intrauterine growth restriction at term1

2019 ◽  
Vol 3 (2) ◽  
pp. 867-876 ◽  
Author(s):  
Caitlin N Cadaret ◽  
Robert J Posont ◽  
Kristin A Beede ◽  
Hannah E Riley ◽  
John Dustin Loy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Intrauterine Growth Restriction ◽  
Muscle Growth ◽  
Maternal Blood ◽  
Protein Catabolism ◽  
Fetal Blood ◽  
Intrauterine Growth ◽  
Skeletal Muscle Growth ◽  
Maternal Inflammation

Abstract Maternal inflammation induces intrauterine growth restriction (MI-IUGR) of the fetus, which compromises metabolic health in human offspring and reduces value in livestock. The objective of this study was to determine the effect of maternal inflammation at midgestation on fetal skeletal muscle growth and myoblast profiles at term. Pregnant Sprague-Dawley rats were injected daily with bacterial endotoxin (MI-IUGR) or saline (controls) from the 9th to the 11th day of gestational age (dGA; term = 21 dGA). At necropsy on dGA 20, average fetal mass and upper hindlimb cross-sectional areas were reduced (P < 0.05) in MI-IUGR fetuses compared with controls. MyoD+ and myf5+ myoblasts were less abundant (P < 0.05), and myogenin+ myoblasts were more abundant (P < 0.05) in MI-IUGR hindlimb skeletal muscle compared with controls, indicating precocious myoblast differentiation. Type I and Type II hindlimb muscle fibers were smaller (P < 0.05) in MI-IUGR fetuses than in controls, but fiber type proportions did not differ between experimental groups. Fetal blood plasma TNFα concentrations were below detectable amounts in both experimental groups, but skeletal muscle gene expression for the cytokine receptors TNFR1, IL6R, and FN14 was greater (P < 0.05) in MI-IUGR fetuses than controls, perhaps indicating enhanced sensitivity to these cytokines. Maternal blood glucose concentrations at term did not differ between experimental groups, but MI-IUGR fetal blood contained less (P < 0.05) glucose, cholesterol, and triglycerides. Fetal-to-maternal blood glucose ratios were also reduced (P < 0.05), which is indicative of placental insufficiency. Indicators of protein catabolism, including blood plasma urea nitrogen and creatine kinase, were greater (P < 0.05) in MI-IUGR fetuses than in controls. From these findings, we conclude that maternal inflammation at midgestation causes muscle-centric fetal programming that impairs myoblast function, increases protein catabolism, and reduces skeletal muscle growth near term. Fetal muscle sensitivity to inflammatory cytokines appeared to be enhanced after maternal inflammation, which may represent a mechanistic target for improving these outcomes in MI-IUGR fetuses.

Acetate as a metabolic substrate in the fetal lamb

1976 ◽  
Vol 230 (2) ◽  
pp. 357-361 ◽  
Author(s):  
VC Char ◽  
RK Creasy
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Maternal Blood ◽  
Mean Value ◽  
Fetal Blood ◽  
Blood Samples ◽  
Metabolic Substrate ◽  
Acetate Concentration ◽  
Fetal Lamb ◽  
The Mean

Fetal acetate metabolsim was studied in chronically catheterized fetal lambs of 110-141 days' gestation. Acetate concentration was measured enzymatically in whole blood drawn simultaneously from maternal and fetal pre- and postplacental vessels. The oxygen content of the fetal blood samples was also measured. Fetal umbilical venous acetate concentration was found to be proportional to the maternal arterial acetate concentration and had a mean value of 0.366 mM. Fetal blood acetate increased significantly, by a mean of 0.081 mM, during circulation through the placenta. This increase was proportional to both the maternal acetate concentration and the concentration gradient of acetate across the placenta. The mean maternal arterial acetate concentration was 1.153 mM. Maternal blood lost significant amounts of acetate, 0.112 mM, during circulation through the uterus and appeared to be the source of the acetate being gained by the fetus. It is estimated that a total of 23 mmol of acetate/kg of fetal weight is being taken up by the fetus each day, providing it with 0.560 g of carbon/kg. Comparisons of acetate uptake with fetal oxygen uptake indicate 10% of the daily fetal oxygen consumption would be required to completely oxidize the acetate being gained by the fetus.

Pharmacokinetics of ethanol and its metabolite, acetaldehyde, and fetolethality in the third-trimester pregnant guinea pig for oral administration of acute, multiple-dose ethanol

1986 ◽  
Vol 64 (8) ◽  
pp. 1060-1067 ◽  
Author(s):  
David W. Clarke ◽  
Nancy A. E. Steenaart ◽  
Christopher J. Slack ◽  
James F. Brien
Keyword(s):  
Guinea Pig ◽  
Amniotic Fluid ◽  
Ethanol Concentration ◽  
Fetal Brain ◽  
Maternal Blood ◽  
Time Interval ◽  
Gas Liquid Chromatography ◽  
Fetal Blood ◽  
Third Trimester ◽  
The Third

The pharmacokinetics of ethanol and its metabolite, acetaldehyde, were determined in the third-trimester pregnant guinea pig (56–59 days gestation) for oral intubation of four doses of 1 g ethanol/kg maternal body weight, administered at 1-h intervals. Animals (n = 4–7) were sacrificed at each of selected times during the 26-h study. Ethanol and acetaldehyde concentrations were determined by headspace gas-liquid chromatography. The maternal and fetal blood ethanol concentration–time curves were virtually superimposable, which indicated unimpeded bidirectional placental transfer of ethanol in the matemal–fetal unit. The blood and brain ethanol concentrations were similar in each of the maternal and fetal compartments during the study, which indicated rapid equilibrium distribution of ethanol. There was accumulation of ethanol in the amniotic fluid resulting in higher ethanol concentration compared with maternal and fetal blood during the elimination phase, which indicated that the amniotic fluid may serve as a reservoir for ethanol in utero. Acetaldehyde was measurable in all the biological fluids and tissues at concentrations that were at least 1000-fold less than the respective ethanol concentrations and were variable. There was ethanol-induced fetolethality that was delayed and variable among animals, and was 55% at 23 h. At this time interval, the ethanol concentrations in maternal blood and brain, fetal brain, and amniotic fluid were 35- to 53-fold greater and the acetaldehyde concentrations in maternal blood and fetal brain were four- to five-fold higher in the animals with dead fetuses compared with the guinea pigs with live litters. These data indicated that decreased ethanol elimination from the maternal–fetal unit was related temporally to the fetolethality.

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