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W W Hay

Publications and source records attributed to W W Hay.

At least 91 records · Page 5Linked to original sources
PubMed1990

Placental-fetal glucose exchange and placental glucose consumption in pregnant sheep.

To determine the separate effects of changes in fetal glucose and insulin concentrations on uteroplacental glucose transfer (UPGT) and consumption (UPGC) we studied 24 late-gestation pregnant sheep during fetal insulin infusions alone and with simultaneous glucose clamp. Insulin infusion alone increased fetal glucose utilization rate (GUR) by 45% (P less than 0.001), decreasing fetal glucose concentration by 40% (P less than 0.01) and thereby increasing fetal glucose clearance (Clglu) by 150% (P less than 0.001). Maternal-fetal glucose gradient also increased, resulting in a 40% increase (P less than 0.02) in UPGT [measured as umbilical glucose uptake (UGU)] and a 30% decrease (P less than 0.05) in UPGC. Addition of a fetal glucose clamp returned fetal glucose concentration to base line and restored UPGC and UGU to control values with a further 2.25-fold increase in fetal GUR. Clglu did not change, as the increase in GUR was proportional to the increase in fetal glucose concentration. Similarly, in animals receiving an insulin infusion plus glucose clamp throughout, maternal glucose concentration, fetal glucose concentration, UPGC, and UGU did not change, whereas GUR and Clglu increased approximately 1.9-fold. These changes were noted at constant maternal glucose concentration and uterine glucose uptake. Thus variation in fetal glucose concentration rather than fetal insulin concentration directly regulates uteroplacental glucose transfer and consumption, whereas both fetal insulin and glucose affect, in separate ways, fetal glucose utilization and clearance.

Animals↗
PubMed1990

Fetoplacental deamination and decarboxylation of leucine.

Fetal and placental metabolism of leucine (Leu) and ketoisocaproic acid (KIC) were studied in seven fetal lambs at 132 +/- 1.3-days gestation. Fetal infusions of [1-13C]Leu, [1-14C]Leu, and antipyrine were carried out for 4 h. Uterine and umbilical blood flows were measured using the antipyrine steady-state diffusion technique. Leu and KIC concentrations, [14C]Leu-specific activities, 14CO2, [13C]Leu, and [13C]KIC enrichment (mole percent enrichment) were measured in the maternal artery, uterine vein, and umbilical artery and vein to calculate net fluxes of tracee and tracer molecules between fetus and placenta and between the uteroplacenta and the maternal circulation. There were net Leu and KIC fluxes into the fetus from the placenta with the KIC flux equal to approximately 19% of the combined Leu plus KIC flux. In addition, there was a net KIC flux into the uterine circulation. The fraction of infused tracer Leu escaping the placenta into the mother was small (approximately 6%). By contrast, there was a rapid exchange of tracer Leu carbon between placenta and fetus resulting in a significant flux of labeled KIC from placenta to fetus. Approximately 20% of the infused tracer carbon was converted to CO2 within the fetus. This rate of conversion was greater than 80% of the total fetoplacental conversion rate and significantly higher than the flux of KIC tracer carbon from placenta to fetus. Fetal KIC decarboxylation rate, calculated from the fetal KIC enrichment data, was 2.83 +/- 0.40 mumol.min-1.kg fetus-1 and approximately 60% of the combined net Leu and KIC flux into the fetus from the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effect of hypoinsulinemia and hyperglycemia on fetal glucose utilization.

The present studies were performed to determine the effect of normal levels of insulin on fetal glucose metabolism and to measure the acute changes in insulin secretion and concentration that occur in response to a hyperglycemia stimulus. In fetal sheep, infusion of somatostatin alone decreased fetal insulin concentration 4 microU/ml (33%) from the basal value without a significant change in fetal glucose concentration, umbilical glucose uptake (UGU), or fetal glucose utilization rate (GUR). Glucose plus somatostatin infusion produced a significantly lower insulin concentration (54% lower, P less than 0.005) and GUR (22% lower, P less than 0.05) at glucose concentration approximately 40 mg/dl compared with glucose infusion alone. No significant difference was seen at glucose concentration of approximately 30 mg/dl. These results indicate that fetal glucose metabolism is responsive not only to changes in glucose but also insulin concentrations; however, a relatively large change in insulin (greater than 5 microU/ml) is necessary to produce a measurable response. These quantitative aspects of fetal insulin effect must be considered when assessing the role of insulin in the regulation of fetal glucose metabolism.

Animals↗
PubMed1990

Model of placental glucose consumption and glucose transfer.

Net ovine uteroplacental glucose consumption (Ro,up) and transfer rates to the fetus (Rf,up) were measured at different concentrations of maternal (GA) and fetal (Ga) arterial plasma glucose that were set and maintained independently by a glucose clamp procedure. Five GA/Ga combinations were studied: 70/15, 70/20, 70/30, 50/14, and 50/24 mg/dl. Rf,up was inversely related to Ga both at GA = 70 and GA = 50. Linear regression analysis of Rf,up vs. Ga for the GA = 70 and GA = 50 groups of observations revealed similar slopes (-0.286 +/- 0.012 vs. -0.217 +/- 0.028 dl.min-1.kg fetus-1) but a significantly higher intercept for the GA = 70 group (10.3 +/- 0.12 vs. 5.5 +/- 0.47 mg.min-1.kg fetus-1). In contrast, Ro,up increased significantly in response to an increase of Ga and had no significant dependence on GA. These results indicate that uteroplacental glucose metabolism occurs primarily in tissues that have direct access to glucose molecules carried by the umbilical circulation and that the glucose transport capacity of the placental barrier is greater on its fetal than its maternal surface. Uteroplacental glucose metabolic rate and its dependence on fetal glucose concentration are major factors that determine the magnitude and variability of the glucose concentration gradient (and thus the rate of net glucose transfer) between maternal and fetal plasma.

Animals↗
PubMed1989

The effects of streptozotocin on rates of glucose utilization, oxidation, and production in the sheep fetus.

Streptozotocin was injected into chronically catheterized, late gestation fetal sheep to produce hypoinsulinemia and to investigate the effects of hypoinsulinemia on the rates of utilization and production of glucose. Each fetus received two IV doses of streptozotocin (100 mg/kg estimated fetal weight per dose). Experiments were conducted before and five to six days after giving the streptozotocin. Experiments consisted of direct measurement of fetal glucose utilization rate (using [U-14C]glucose tracer) and umbilical glucose uptake rate (Fick principle) during basal and glucose infusion periods. Fetal endogenous production rate was calculated as the difference between rates of fetal glucose utilization and umbilical glucose uptake. Following streptozotocin injections the rate of fetal glucose utilization was reduced (5.50 +/- 0.34 to 4.13 +/- 0.32 mg/kg/min) as was the rate of fetal CO2 production from fetal glucose carbon oxidation (91.7 +/- 5.3 to 71.7 +/- 6.0 mumol/kg/min) and the rate of fetal glucose oxidation (2.75 +/- 0.16 to 2.15 +/- 0.18 mg/kg/min). At the same time the rate of fetal endogenous glucose production was enhanced (0.31 +/- 0.18 to 2.06 +/- 0.28 mg/kg/min). These changes in glucose metabolism were accompanied by hypoinsulinemia (16 +/- 2 to 8 +/- 1 muU/mL), an inhibition of insulin secretion in response to glucose infusion (16 +/- 2 to 34 +/- 2 muU/mL control, 8 +/- 1 to 9 +/- 1 muU/mL after streptozotocin), hyperglycemia (19.5 +/- 0.7 to 30.4 +/- 1.7 mg/dL), and a reduction in the rate of umbilical glucose uptake (5.19 +/- 0.34 to 2.07 +/- 0.40 mg/kg/min). The disturbances in glucose metabolism could be alleviated only in part by insulin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Clinical application of a new glucose analyzer in the neonatal intensive care unit: comparison with other methods.

We evaluated the operation of the Yellow Springs Instrument Co. (YSI) glucose analyzer (model 23A) by clinical nurses for the measurement of blood glucose in the intensive care nursery. In vitro performance was determined with the use of aqueous standards; with a 2-point calibration of 0.0 and 200 mg/dl, a precision of better than 1.0% of each standard (25, 50, 100, 200 mg/dl) was achieved, and the linearity was excellent (Y = 0.99X - 0.49, r = 0.99). The YSI correlated well with a manual spectrophotometric glucose oxidase method (r = 0.99) and the Kodak Ektachem analyzer (r = 0.98) using human umbilical cord blood samples. Five trained clinical nurses performed all YSI and glucose reagent strip analyses, including all in vitro and patient samples. Four reagent strip methods were compared with the YSI from 104 neonatal heel-stick blood samples: Glucometer II with memory (r = 0.73), Glucostix (r = 0.74), Dextrostix (r = 0.70), and Chemstrip bG (r = 0.83). We conclude that clinical nurses can and do learn to use the YSI with excellent precision and that the YSI represents an improved method for measuring glucose concentrations in the newborn intensive care nursery.

Blood Chemical Analysis↗
PubMed1989

Effects of glucose and insulin on fetal glucose oxidation and oxygen consumption.

Glucose and insulin clamp experiments were performed in late-gestation fetal lambs to quantify the separate and combined effects of physiological concentrations of fetal glucose (G; 7.3-62.6 mg/dl) and insulin (I; 2-119 uU/ml) on fetal glucose metabolism and O2 consumption. Fetal glucose utilization rate (GUR) varied from 2.82 to 15.12 mg.min-1.kg-1. Fetal CO2 production from fetal glucose carbon oxidation (CO2Pr) varied from 32 to 234 mumol.min-1.kg-1 and was directly related to G and I [CO2Pr = -0.00868 + 0.00578 (G) + 0.000901 (I) - 0.0000619 (G)2, r = 0.88] and to GUR (CO2Pr = 0.0159 GUR - 0.0130, r = 0.89). CO2Pr accounted for 54.7% of the mean GUR and for 35.9% of the mean umbilical O2 uptake (UO2U), ranging from 26.0% in the control studies to 36.5% in hyperinsulinemic-euglycemic studies and to 45.1% in hyperinsulinemic-hyperglycemic studies. UO2U varied from 0.200 to I [UO2U = 0.303 + [0.000813 (G)] + [0.0000461 (I)], r = 0.89] and to GUR (UO2U = 0.0098 GUR + 0.275, r = 0.91). These results define independent (additive) effects of G and I on glucose oxidation in the late gestation fetal lamb and demonstrate the necessity for considering the levels of both G and I when studying these aspects of fetal metabolism.

Animals↗
PubMed1989

Regulation of placental glucose transfer and consumption by fetal glucose production.

We studied ten normoglycemic [maternal glucose (GA) = 70 mg/dL] and six insulin-induced hypoglycemic (GA = 22 mg/dL) pregnant sheep to test the hypothesis that development of fetal glucose production (GPR) could help maintain fetal glucose concentration, limit uteroplacental-fetal glucose transfer (UPGT), and sustain uteroplacental glucose consumption (UPGC). Compared with the normoglycemic group, the hypoglycemic group demonstrated the following values: fetal glucose concentration (Ga) was 9.8 +/- 0.8 mg/dL (51% lower, p less than 0.01), uterine glucose uptake (UtGU) was 16.7 +/- 1.4 mg/min (54% lower, p less than 0.01), UPGT was 3.1 +/- 0.6 mg/min (81% lower, p less than 0.001), and UPGC was 13.6 +/- 1.4 mg/min (30% lower, p less than 0.05). The reduction in UPGC was significantly less (p less than 0.05) than the reductions in UPGT and UtGU. Fetal glucose utilization rate (GUR) was decreased 20% (p less than 0.05) to 3.99 +/- 0.35 mg/min/kg. A further decrease in GUR was prevented by the appearance of fetal GPR of 2.82 +/- 0.32 mg/min/kg (p less than 0.05) compared with negligible GPR in the normoglycemic group. UPGT and UPGC in both groups were not influenced by maternal or fetal insulin infusions as long as Ga did not change; however, fetal glucose infusion that increased Ga increased UPGC in both groups. We conclude that, during chronic maternal hypoglycemia, increased fetal GPR limits the simultaneous decrease in fetal GUR and glucose concentration. By sustaining Ga fetal GPR limits UPGT to a significantly greater extent than UtGU, diverting UtGU to UPGC. Thus, fetal GPR promotes placental as well as fetal metabolic autonomy when the maternal supply of glucose is reduced.

Animals↗
PubMed1989

Effect of maternal glucose concentration on uteroplacental glucose consumption and transfer in pregnant sheep.

The present study was designed to measure the relationships between maternal arterial glucose concentration [( GI]A) and fetal arterial glucose concentration [( GI]a), uteroplacental glucose consumption (UPGC), and the rate of uteroplacental glucose transfer to the fetus (UPGT) in pregnant sheep in late gestation. [GI]A was controlled by a glucose clamp technique and the glucose flux rates of the uteroplacenta were quantified by the Fick principle. [GI]A varied from 1.81 to 154.7 mg/dl; [GI]a was directly related to [GI]A: [GI]a = 0.374 [GI]A + 1.81, r = 0.873, P less than 0.001. Fetal arterial blood oxygen content decreased with [GI]A (P less than 0.05) and fetal arterial blood lactate concentration increased with [GI]A (P less than 0.001). There was no significant effect of [GI]A on the rates of uteroplacental lactate production, uteroplacental oxygen consumption, fetal oxygen consumption, or uterine or umbilical blood flow. Both UPGC and UPGT were directly related to [GI]A: UPGC = -2.221 x 10(-3) chi 2 + 0.646 x -6.016, r = 0.80; UPGT = -1.208 x 10(-3) chi 2 + 0.405 x -2.416, r = 0.90. UPGC and UPGT were approximately parallel over the range of [GI]A studied (UPGC = 1.19 UPGT + 3.79, r = 0.764). These results demonstrate the importance of UPGC to maternal-fetal glucose homeostasis and indicate that factors regulating uteroplacental glucose consumption and transfer to the fetus become limiting at comparable levels of [GI]A and [GI]a. The estimated kinetic constants for UPGC represent the metabolism of glucose by the uteroplacental tissues, but the estimated kinetic constants for UPGT represent the metabolism of glucose by the fetus as well as the transfer of glucose by the uteroplacenta to the fetus.

Animals↗
PubMed1989

Neonatal pulse oximetry: accuracy and reliability.

Pulse oximetry has gained widespread use in neonatal oxygen monitoring. However, because specific morbidity in neonates has been related to abnormal levels of oxygen partial pressure (PaO2), it is essential to demonstrate that pulse oxygen saturation values (SpO2) are highly accurate and reflect with precision the simultaneous PaO2. In this report, data is presented that describe the accuracy of the Ohmeda Biox 3700 pulse oximeter. SpO2 was highly correlated with arterial blood oxygen saturation (r = .99) measured on arterial (catheter) blood using a two-wavelength Radiometer OSM2 Hemoximeter. When compared with PaO2, SpO2 values of 92% +/- 3% (mean +/- range) excluded all of the measured PaO2 values less than 45 mm Hg and greater than 100 mm Hg. SpO2-tcPO2 (transcutaneous PO2) and SpO2-PaO2 (catheter or percutaneous arterial PO2) correlations showed that bronchopulmonary dysplasia, percutaneous arterial sampling, and nipple feeding skewed the tcPO2 but not the PaO2 correlations with SpO2, indicating that SpO2 is not sensitive to peripheral factors that affect tcPO2. SpO2-PaO2 correlation was not affected by gestational age. A high degree of accuracy of SpO2 values and SpO2 prediction of normal appearing PaO2 values are defined by these results.

Blood Gas Monitoring, Transcutaneous↗
PubMed1988

The effects of pancreatectomy on the rates of glucose utilization, oxidation and production in the sheep fetus.

The effects of fetal pancreatectomy on the uptake and metabolism of glucose were investigated in chronically catheterized sheep fetuses during late gestation by using tracer methodology. Rates of glucose uptake and metabolism were also measured in pancreatectomized fetuses during the infusion of insulin. Pancreatectomy produced hypoinsulinaemia and significantly reduced the rates of fetal glucose utilization and umbilical glucose uptake in comparison to intact fetuses of a similar gestational age. There was no significant alteration in the glucose oxidation fraction after pancreatectomy but because glucose utilization was low in the pancreatectomized fetuses, the rate of fetal glucose oxidation was significantly less after pancreatectomy than in intact animals. No apparent endogenous production of glucose was observed in the pancreatectomized fetuses. Insulin infusion into the pancreatectomized fetuses raised the rates of umbilical glucose uptake and of fetal glucose utilization and oxidation by 40-50% to values similar to those observed in intact animals. The endogenous production of glucose remained negligible during the infusion of insulin into the pancreatectomized fetuses. There was a net flux of radioactive glucose from the pancreatectomized fetus to the uteroplacental tissues and from the uteroplacental tissues into the uterine circulation. These net fluxes and the rate of placental metabolism of tracer glucose decreased significantly during the infusion of insulin into the pancreatectomized fetus. When all the data were combined, partial correlation analyses of the net uteroplacental uptake of tracer glucose and the fetal concentrations of plasma insulin and blood glucose showed that the fetal arterial glucose concentration was the major influence on the net flux of tracer from the fetus to the uteroplacental tissues. These observations demonstrate that the endogenous concentration of insulin has an important role in regulating glucose metabolism in sheep fetus during late gestation.

Animals↗
PubMed1988

Effects of insulin and glucose concentrations on glucose utilization in fetal sheep.

Glucose and insulin clamp experiments were performed in vivo in chronically catheterized, late-gestation fetal lambs to quantify the effects of glucose and insulin on fetal glucose metabolism. Fetal glucose uptake from the placenta via the umbilical circulation (umbilical glucose uptake) was measured by application of the Fick principle, and fetal glucose utilization rate (GUR) was measured using [U-14C]glucose tracer. Fetal plasma insulin concentrations ranged from 2 to 119 microU.ml-1 and fetal blood glucose concentrations ranged from 7.3 to 62.6 mg.dl-1. GUR varied from 2.82 to 15.12 mg/min/kg and the exogenous glucose entry rate (umbilical glucose uptake + glucose infusion) varied from 2.46 to 13.95 mg/min/kg. The mean GUR [6.53 +/- 0.28 (SEM) mg/kg/min] was not different from the mean exogenous glucose entry rate [6.29 +/- 0.30 (SEM) mg/kg/min]. Multiple linear regression analysis on a glucose-by-insulin surface demonstrated a best-fit model of fetal glucose utilization following the quadratic equation: GUR = -0.322 + [0.289 (glucose)] + [0.108 (insulin)] - [0.00319 (glucose)2] - [0.000673 (insulin)2], r = 0.883 (all terms significant at p less than 0.02). This model predicted a GURmax of 10.56 mg/min/kg at blood glucose concentration = 45.3 mg/dl and plasma insulin concentration = 80 microU/ml and Km values for blood glucose concentration and plasma insulin concentration of 20.6 mg/dl and 10 microU/ml, respectively. According to this model, the glucose and insulin effects were additive. Furthermore, change in GUR was not proportionate to change in glucose concentration, accounting for a decreasing metabolic clearance rate at higher glucose concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Use of fetal streptozotocin injection to determine the role of normal levels of fetal insulin in regulating uteroplacental and umbilical glucose exchange.

The present study was performed to determine the role of the normal fetal concentration of insulin in regulating placental-fetal glucose exchange. Fetal insulin deficiency was produced by streptozotocin injection into near term fetal sheep, and the effects of this insulin deficiency on net uteroplacental glucose uptake and net umbilical glucose uptake were measured. Each fetus received two or three doses of streptozotocin, 100 mg.kg-1.dose-1, given on separate days. This dosage of streptozotocin produced a 97.6% reduction in fetal pancreatic insulin content, a fall in fetal plasma insulin concentration (21 +/- 2 to 10 +/- 1 microU.ml-1), a rise in fetal plasma glucagon concentration (57 +/- 4 to 114 +/- 19 pg.ml-1), a rise in fetal blood glucose concentration (20.4 +/- 0.9 to 33.4 +/- 4.4 mg.dl-1), and a failure of insulin secretion in response to glucose infusion. Fetal blood oxygen content and umbilical oxygen uptake were normal and did not change during the entire study. Umbilical glucose uptake was reduced by 66% (5.98 +/- 0.38 to 2.02 +/- 1.31 mg.min-1.kg-1) after the streptozotocin-induced hypoinsulinemia and hyperglycemia but was returned to the control level by an insulin infusion into the fetus that reestablished the control maternal to fetal glucose concentration gradient. Net uteroplacental glucose uptake (consumption) did not change throughout the study. Because glucose concentration and umbilical glucose uptake could be normalized by an insulin infusion, it is unlikely that direct or toxic effects of streptozotocin on fetal or placental glucose metabolism were primarily responsible for the hyperglycemia and the reduced rate of umbilical glucose uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of high levels of insulin on glucose utilization and glucose production in pregnant and nonpregnant sheep.

The present study was conducted to test the hypothesis that pregnancy in sheep alters the effects of insulin on glucose utilization and glucose production. Euglycemic, hyperinsulinemic glucose clamp experiments were performed in chronically catheterized, unstressed, fed or 24-hr fasted, nonpregnant sheep and fed, pregnant sheep. Endogenous glucose production rate for the whole sheep and glucose utilization rate of the uterine and nonuterine maternal tissues were measured in control and high-insulin periods by tracer technique using [6-3H]glucose. Control glucose utilization rate in the fed, nonpregnant sheep was significantly (P less than 0.05) greater than that in the fasted, nonpregnant sheep, 2.29 +/- 0.17 and 1.86 +/- 0.11 mg/min/kg, respectively, and also in the nonuterine maternal tissues of the pregnant sheep (1.71 +/- 0.18 mg/min/kg). Insulin stimulated glucose utilization 116.4 +/- 14.8% in the fed, nonpregnant sheep but only 82.8 +/- 11.0% in the fasted, nonpregnant sheep and 94.2 +/- 14.3% in the nonuterine tissues of the fed, pregnant sheep. Also, insulin suppressed endogenous glucose production to 53.2 +/- 5.6% in the fed, nonpregnant sheep, to 3.9 +/- 3.1% in the fasted, nonpregnant sheep, and to 9.0 +/- 3.7% in the fed, pregnant sheep. In the pregnant animals, uterine glucose uptake and uterine glucose utilization were not different and were not altered by changes in maternal insulin concentration. The results indicate that during late pregnancy glucose utilization is reduced and resistance to the effect of insulin to enhance glucose utilization is present in the nonuterine maternal tissues compared with nonpregnant, fed sheep. In contrast, the effectiveness of insulin to suppress glucose production in the pregnant sheep is greater than that in nonpregnant, fed sheep. These results also demonstrate that differential changes in the effect of insulin can exist simultaneously between peripheral (glucose consuming) and central (glucose producing) tissues. The changes in glucose utilization and in insulin effect in the pregnant sheep are both qualitatively and quantitatively similar to those of the nonpregnant sheep when fasted, suggesting that similar substrate and/or hormonal factors may be involved.

Animals↗
PubMed1987

Leucine disposal and oxidation rates in the fetal lamb.

To verify previous indirect evidence suggesting an important role of amino acids as substrates of fetal oxidative metabolism, leucine disposal and oxidation rates were measured in chronically catheterized fetal lambs during the last month of gestation. Under normal physiologic conditions the leucine oxidation rates were 6.43 +/- 1.02 mumol min-1 for fetuses with an average weight of 3.22 +/- 0.07 kg and comparable in magnitude to the fetal rate of leucine accretion. In seven animals studied before and during fasting, the fetal leucine oxidation rate increased with fasting from 5.8 +/- 1.0 to 10.8 +/- 1.3 mumol min-1. These data demonstrate that there is rapid oxidative degradation of leucine by the fetus and that the rate of this process increases in response to maternal fasting.

Animals↗
PubMed1987

Fructose disposal and oxidation rates in the ovine fetus.

Fructose disposal and oxidation rates were measured in fetal lambs receiving a constant intravenous infusion of D-[U-14C]fructose. Approximately 60% of the infused tracer entered the placenta, but loss of fructose into the maternal circulation was negligible. Fructose was metabolized to lactate and CO2 in both the placenta and fetus, whereas there was no detectable conversion to glucose. In well-fed ewes the fetal disposal and utilization rates of fructose were 2.4 +/- 0.17 and 0.97 +/- 0.09 mg/min. kg, respectively. The umbilical excretion rate of CO2 originating from the oxidation of fetal fructose was 18.1 +/- 1.3 mumol/min. kg or 5.3% of total fetal CO2 production. This excretion rate is one-fifth of the CO2 excretion rate from fetal glucose carbon. In four ewes comparison of fructose metabolism in the fed and fasted states showed a significant decrease of fructose production and oxidation with fasting. Although fructose is present in high concentrations in the fetal blood of ungulates, its contribution to fetal oxidative metabolism is relatively small in comparison to glucose.

Animals↗