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Academic literature on the topic 'Uterine glucose uptake'
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Journal articles on the topic "Uterine glucose uptake"
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Chandler, K. D., B. J. Leury, A. R. Bird, and A. W. Bell. "Effects of undernutrition and exercise during late pregnancy on uterine, fetal and uteroplacental metabolism in the ewe." British Journal of Nutrition 53, no. 3 (May 1985): 625–35. http://dx.doi.org/10.1079/bjn19850072.
Full textAbstract:
1. Uterine, umbilical and, by difference, uteroplacental net uptakes of oxygen, glucose, lactate and 3-hydroxybutyrate (uterine uptake only) were measured in single-pregnant ewes which were either well-fed throughout, or severely undernourished for 8–20 d during late pregnancy. All animals were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min.2. Undernutrition did not significantly affect fetal or placental weights at 143 d gestation but caused a 14% decrease in maternal live weight. Uterine blood flow was decreased by 32% and was associated with a significant decrease in uteroplacental oxygen uptake; neither umbilical blood flow nor fetal O2, uptake were affected by maternal plane of nutrition. Maternal and fetal hypoglycaemia in underfed ewes was accompanied by 46–63 % decreases in uterine, umbilical and uteroplacental net uptakes of glucose, and similar declines in uterine and umbilical glucose/O, quotients. Moderate maternal hyperketonaemia was associated with 2.5-fold and 3-fold increases in uterine net uptake of 3-hydroxybutyrate and 3-hydroxybutyrate/O2 quotient respectively.3. Exercise caused significant decreases in uterine blood flow in fed and underfed ewes but did not affect uterine or umbilical O2 uptakes; uterine net glucose uptake increased in most ewes but umbilical uptake was not significantly affected. Umbilical net uptake of lactate was significantly reduced. In underfed ewes, the extent of hyperketonaemia was significantly reduced by exercise.4. Contrary to earlier proposals, the ovine pregnant uterus is sensitive and adaptable to long- and short-term alterations in maternal energy balance, as achieved by chronic undernutrition and exercise respectively. Thus, the fetus and placenta significantly add to, but do not necessarily have priority over the energy demands of other tissues of the ewe.
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Leury, B. J., A. R. Bird, K. D. Chandler, and A. W. Bell. "Glucose partitioning in the pregnant ewe: Effects of undernutrition and exercise." British Journal of Nutrition 64, no. 2 (September 1990): 449–62. http://dx.doi.org/10.1079/bjn19900045.
Full textAbstract:
Maternal whole-body glucose entry rate and uterine and umbilical net uptakes of glucose and oxygen were measured in single-pregnant ewes which were either well-fed throughout, or fed at 0.3–0.4 predicted energy requirement for 7–21 d during late pregnancy. All ewes were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min. Underfed ewes suffered significant decreases in live weight and had lower fetal, but not placental, weights at 140–144 d gestation. Undernutrition also caused large decreases in maternal glycaemia and glucose entry rate, which were associated with equally large decreases in uterine and umbilical net uptakes and O2 quotients of glucose, and with a decrease in placental glucose transfer capacity. Exercise caused increases in maternal blood concentration, entry rate and uterine net uptake of glucose, the magnitudes of which were not significantly affected by plane of nutrition. Umbilical glucose uptake and placental glucose transfer capacity increased during exercise in underfed but not fed ewes. The fractional distribution of maternal glucose to the pregnant uterus, and of uterine glucose uptake to the fetus, were unaltered by undernutrition; during exercise, a disproportionately small fraction of the increased maternal glucose supply went to the uterus. The results confirm that the ovine conceptus responds to nutritional reduction in maternal glucose availability in a manner similar to non-uterine maternal tissues. Major reductions in glucose supply appear to override putative glucose-sparing mechanisms which may operate to favour the conceptus in better-nourished animals.
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Bell, A. W., J. M. Kennaugh, F. C. Battaglia, E. L. Makowski, and G. Meschia. "Metabolic and circulatory studies of fetal lamb at midgestation." American Journal of Physiology-Endocrinology and Metabolism 250, no. 5 (May 1, 1986): E538—E544. http://dx.doi.org/10.1152/ajpendo.1986.250.5.e538.
Full textAbstract:
Uterine and umbilical blood flows, the placental clearance of 3H2O, uterine and umbilical uptakes of oxygen, glucose, and lactate were measured in conscious, pregnant sheep at 71-81 days gestation. Fetal weight was 210 +/- 20 g and less than half placental weight. In relation to fetal weight, umbilical flow was 468 +/- 57 ml X min-1 X kg-1, more than double normal values for the mature fetus. Clearance of 3H2O was approximately 12% of the late pregnancy value but high in relation to fetal weight (280 +/- 23 ml X min-1 X kg-1). Fetal oxygen uptake was 10.9 +/- 0.6 ml X min-1 X kg-1, approximately 40% greater than in late gestation. Umbilical uptake of glucose was also relatively high, whereas lactate uptake was low. Uteroplacental tissues consumed more than 80% of the oxygen and glucose taken up by the pregnant uterus. However, uteroplacental utilization rates of oxygen and glucose as well as net lactate production were lower (approximately 50, 30, and 25%, respectively) than in late pregnancy, despite a larger placental mass (486 +/- 22 vs. 302 +/- 12 g).
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Das, Utpala G., Jing He, Richard A. Ehrhardt, William W. Hay, and Sherin U. Devaskar. "Time-dependent physiological regulation of ovine placental GLUT-3 glucose transporter protein." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2252—R2261. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2252.
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We immunolocalized the GLUT-3 glucose transporter isoform versus GLUT-1 in the late-gestation epitheliochorial ovine placenta, and we examined the effect of chronic maternal hyperglycemia and hypoglycemia on placental GLUT-3 concentrations. GLUT-3 was limited to the apical surface of the trophoectoderm, whereas GLUT-1 was on the basolateral and apical surfaces of this cell layer and in the epithelial cells lining the placental uterine glands. GLUT-3 concentrations declined at 17–20 days of chronic hyperglycemia ( P < 0.05), associated with increased uterine and uteroplacental net glucose uptake rate, but a normal fetal glucose uptake rate was observed. Chronic hypoglycemia did not change GLUT-3 concentrations, although uterine, uteroplacental, and fetal net glucose uptake rates were decreased. Thus maternal hyperglycemia causes a time-dependent decline in the entire placental glucose transporter pool (GLUT-1 and GLUT-3). In contrast, maternal hypoglycemia decreases GLUT-1 but not GLUT-3, resulting in a relatively increased GLUT-3 contribution to the placental glucose transporter pool, which could maintain glucose delivery to the placenta relative to the fetus when maternal glucose is low.
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Hooper, S. B., D. W. Walker, and R. Harding. "Oxygen, glucose, and lactate uptake by fetus and placenta during prolonged hypoxemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 2 (February 1, 1995): R303—R309. http://dx.doi.org/10.1152/ajpregu.1995.268.2.r303.
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Our aim was to compare the effects of short (4 h) and prolonged (24 h) periods of reduced uterine blood flow (RUBF) on fetal and placental uptake of O2, glucose, and lactate. In pregnant sheep, uterine and umbilical blood flows were measured under normal conditions and after 4 and 24 h of RUBF. A 50% reduction in uterine blood flow caused a 56% reduction in fetal arterial O2 saturation (SaO2). Umbilical blood flow increased from 325 +/- 33 to 378 +/- 32 ml.min-1.kg-1 (P < 0.05) after 4 h but was not different from pre-RUBF values after 24 h. O2 uptake by the gravid uterus was not altered by RUBF, due to an increase (84%) in uterine O2 extraction. Similarly, uteroplacental and fetal O2 consumptions and fetal glucose uptake were not affected by RUBF, whereas uteroplacental glucose uptake was significantly reduced after 4 h (by 42%) and 24 h (by 58%) of RUBF. Fetal lactate uptake was greatly reduced from 78.7 +/- 15.5 to -167 +/- 57 mumol.min-1.kg-1 after 4 h and to -198 +/- 80 mumol.min-1.kg-1 after 24 h of RUBF; negative values indicate placental lactate uptake from the fetal circulation. Thus, although RUBF significantly reduced fetal SaO2, fetal and uteroplacental O2 consumptions did not change. In addition, although fetal glucose uptake was not altered by RUBF, during RUBF the placenta became a major site of lactate clearance from the fetal circulation.
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Reynolds, L. P., C. L. Ferrell, Debra A. Robertson, and S. P. Ford. "Metabolism of the gravid uterus, foetus and utero-placenta at several stages of gestation in cows." Journal of Agricultural Science 106, no. 3 (June 1986): 437–44. http://dx.doi.org/10.1017/s0021859600063309.
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SummaryTo quantify changes in rates of metabolism and nutrient uptake of gravid uteiine, foetal and utero-placental tissues throughout gestation, mature Hereford cows received surgery at 132 ± 0·6 (n = 12), 176 ± 0·5 (n = 8), 220 ±0·4 (n = 11) and 245 ±1·5 (n = 7) days after mating. Indwelling catheters were implanted into a uterine artery and vein of all cows. Foetal catheters also were implanted into an umbilical vein and foetal femoral artery and vein (days 176 and 220) or into a placental artery and two placental veins (days 132 and 245). Approximately 5 days after surgery, deuterium oxide was infused into a foetal femoral venous or placental venous catheter during a 3 h period to quantify uterine and umbilical blood flows by steady-state diffusion methods. Oxygen, glucose, lactate and α-amino acid nitrogen concentrations were determined for uterine and foetal blood samples collected during this procedure.Uterine blood flow increased 4·5-fold (2·92–13·181/min) and umbilical blood flow increased 21-fold (0·28–5·861–min) during the interval of gestation studied. The relative rate of increase of umbilical blood flow was about twice as great as that of uterine blood flow. Uterine arterial and umbilical venous concentrations as well as uterine arterial-venous and umbilical venous-arterial concentration differences in metabolites changed little with stage of gestation. However, because rates of blood flow increased, uptakes of O2, glucose and α-amino N by the gravid uterus and foetus increased as gestation advanced. The proportion of gravid uterine uptakes utilized by the foetus increased from day 137 to 226 for O2 (24–58%) and from day 137 to 180 for glucose (4–19%), then remained relatively constant. The proportion of gravid uterine α-amino N uptake utilized by the foetus remained relatively constant and averaged 60%. A net secretion of lactate from the utero-placenta to the uterine and foetal circulations was observed and increased as gestation advanced. These data indicate that increased rates of uptake or secretion of metabolites by tissues of the gravid uterus can be explained primarily by increased rates of uterine and umbilical blood flows.
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Trotta, Ronald J., Manuel A. Vasquez-Hidalgo, Brandon I. Smith, Sarah A. Reed, Kristen E. Govoni, Kimberly A. Vonnahme, and Kendall C. Swanson. "248 Maternal Nutrient Restriction During Mid-gestation Decreases Uteroplacental Release and Fetal Uptake of Essential Amino Acids in Sheep." Journal of Animal Science 99, Supplement_3 (October 8, 2021): 130–31. http://dx.doi.org/10.1093/jas/skab235.238.
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Abstract To examine the effects of maternal nutrient restriction on net uteroplacental flux during mid-gestation, 14 singleton ewes (48.2 ± 4.0 kg body weight) were fed 100% (control; CON; n = 7) or 60% of nutrient requirements (restricted; RES; n = 7) from day 50–90 (mid-gestation). On day 90, uteroplacental blood flow was measured via Doppler ultrasonography and blood samples were collected from the femoral artery, uterine vein, umbilical artery, and umbilical vein. Blood vessel glucose and amino acids (AA) concentrations were measured and arterial-venous (uterine, AV; fetal, va) differences and net fluxes were calculated. Data were analyzed using the GLM procedure of SAS for effects of treatment. Nutrient restriction during mid-gestation did not influence (P ≥ 0.17) uterine or umbilical blood flows. Uterine AV and fetal va differences of total, essential, and nonessential AA were not influenced (P > 0.10) by nutrient restriction. Nutrient restriction decreased (P ≤ 0.05) uterine and uteroplacental release of total AA and tended to decrease (P = 0.07) total AA uptake by the fetus. Uteroplacental release and fetal uptake of essential AA were decreased (P = 0.03) with RES by 53.4% and 45%, respectively. Uterine and uteroplacental release of nonessential AA were decreased (P = 0.03) with RES but, fetal uptake was not affected (P = 0.14). Nutrient restriction decreased (P ≤ 0.04) fetal uptake of methionine, phenylalanine, threonine, and valine and tended to decrease (P ≤ 0.10) fetal uptake of isoleucine, leucine, and tryptophan. Umbilical artery glucose concentrations were 32% lesser (P = 0.01) with RES and RES tended to increase (P = 0.08) fetal glucose uptake. Nutrient restriction during mid-gestation altered uteroplacental and fetal flux of AA in the current study. The results may indicate that fetal metabolism shifts to adapt to reduced AA supply which results in greater glucose utilization.
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Tanner, Amelia R., Cameron S. Lynch, Victoria C. Kennedy, Asghar Ali, Quinton A. Winger, Paul J. Rozance, and Russell V. Anthony. "CSH RNA Interference Reduces Global Nutrient Uptake and Umbilical Blood Flow Resulting in Intrauterine Growth Restriction." International Journal of Molecular Sciences 22, no. 15 (July 29, 2021): 8150. http://dx.doi.org/10.3390/ijms22158150.
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Deficiency of the placental hormone chorionic somatomammotropin (CSH) can lead to the development of intrauterine growth restriction (IUGR). To gain insight into the physiological consequences of CSH RNA interference (RNAi), the trophectoderm of hatched blastocysts (nine days of gestational age; dGA) was infected with a lentivirus expressing either a scrambled control or CSH-specific shRNA, prior to transfer into synchronized recipient sheep. At 90 dGA, umbilical hemodynamics and fetal measurements were assessed by Doppler ultrasonography. At 120 dGA, pregnancies were fitted with vascular catheters to undergo steady-state metabolic studies with the 3H2O transplacental diffusion technique at 130 dGA. Nutrient uptake rates were determined and tissues were subsequently harvested at necropsy. CSH RNAi reduced (p ≤ 0.05) both fetal and uterine weights as well as umbilical blood flow (mL/min). This ultimately resulted in reduced (p ≤ 0.01) umbilical IGF1 concentrations, as well as reduced umbilical nutrient uptakes (p ≤ 0.05) in CSH RNAi pregnancies. CSH RNAi also reduced (p ≤ 0.05) uterine nutrient uptakes as well as uteroplacental glucose utilization. These data suggest that CSH is necessary to facilitate adequate blood flow for the uptake of oxygen, oxidative substrates, and hormones essential to support fetal and uterine growth.
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Thureen, Patti J., Susan M. Anderson, and William W. Hay. "Regulation of uterine and umbilical amino acid uptakes by maternal amino acid concentrations." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 3 (September 1, 2000): R849—R859. http://dx.doi.org/10.1152/ajpregu.2000.279.3.r849.
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We tested the hypothesis that decreased fetal amino acid (AA) supply, produced by maternal hypoaminoacidemia (low AA) during hyperglycemia (HG), is reversible with maternal AA infusion and regulates fetal insulin concentration ([I]). We measured net uterine and umbilical AA uptakes during maternal HG/low AA concentration ([AA]) and after maternal intravenous infusion of a mixed AA solution. After 5 days HG, all maternal [AA] except glycine were decreased >50%, particularly essential [AA] ( P < 0.00005). Most fetal [AA] also were decreased, especially branched-chain AA ( P < 0.001). Maternal AA infusion increased net uterine uptakes of Val, Leu, Ile, Met, and Ser and net umbilical uptakes of Val, Leu, Ile, Met, Phe, and Arg but did not change net uteroplacental uptake of any AA. Fetal [I] increased 55 ± 14%, P < 0.001, with correction of fetal [AA], despite the lack of change in fetal glucose concentration. Thus generalized maternal hypoaminoacidemia decreases uterine and umbilical uptakes of primarily the essential AA and decreases fetal branched-chain [AA]. These changes are reversed with correction of maternal [AA], which also increases fetal [I].
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Wallace, Jacqueline M., Deirdre A. Bourke, Raymond P. Aitken, Neil Leitch, and William W. Hay. "Blood flows and nutrient uptakes in growth-restricted pregnancies induced by overnourishing adolescent sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 4 (April 1, 2002): R1027—R1036. http://dx.doi.org/10.1152/ajpregu.00465.2001.
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To establish physiological mechanisms for fetal growth restriction in pregnant adolescent ewes we studied uterine, fetal, and uteroplacental metabolism in ewes offered a high ( n = 12) or moderate ( n = 10) dietary intake. High intakes decreased placental (226 vs. 414 g, P < 0.001) and fetal weight (3,323 vs. 4,626 g, P < 0.01). Uterine blood flow was reduced absolutely (−36%) but proportional to conceptus weight; umbilical blood flow was reduced absolutely (−37%) and per fetal weight (−15%). Uterine oxygen uptake was decreased per conceptus weight (−14%); there was no change in fetal weight oxygen consumption. Uteroplacental oxygen consumption and clearance were reduced proportional to weight. Similar changes were measured for glucose fluxes and fetal glucose concentration; fetal insulin concentration was reduced. In this model of fetal growth restriction, therefore, maintenance of fetal weight-specific glucose and oxygen consumption rates are producing relative hypoglycemia and hypoxemia. This indicates that increased fetal glucose clearance and/or insulin sensitivity may be operating as compensatory mechanisms to preserve normal fetal metabolism while fetal growth is sacrificed.
Dissertations / Theses on the topic "Uterine glucose uptake"
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Regnault, Timothy Robert Hume, of Western Sydney Hawkesbury University, Faculty of Agriculture and Horticulture, and School of Agriculture and Rural Development. "Orchestrated partitioning of maternal nutrients during ovine pregnancy." THESIS_FAH_ARD_Regnault_T.xml, 1997. http://handle.uws.edu.au:8081/1959.7/15.
Full textAbstract:
Ovine placental lactogen (oPL) is postulated to be involved in the repartitioning of maternal nutrients during pregnancy, through its effect on insulin metabolism. Ovine pancreatic insulin responses to exogenous glucose are depressed during pregnancy and this depression becomes more pronounced as gestation advances. In addition, under the hormonal environment of rising oPL and growth hormone (oGH) concentrations, maternal whole body glucose irreversible loss (GIL) increases. The percentage of GIL accounted for by uterine glucose uptake also increases with advancing gestation and increasing litter size. Regression analysis of oPL concentration with glucose uterine uptake as a percentage of GIL, accounts for 39% of variation. Maternal oPL concentrations which increase with gestational age, were significantly greater in multiple bearing ewes and ewes subjected to reduced metabolisable energy (ME) intakes. It is postulated that through actions on pancreatic sensitivity, oPL plays a major role as a homeorhetic control during pregnancy. Elevated oPL concentrations were strongly associated with continually depressed pancreatic insulin secretory ability. The reduction in pancreatic sensitivity to glucose was not as a result of elevation in GH or non-esterified fatty acid (NEFA) concentrations. Muscle insulin receptor number and affinity were found to increase with increasing litter size, suggesting that pregnancy associated insulin resistance occurs predominantly in adipose tissue. During ovine pregnancy there is a specific stimulation of maternal gluconeogenesis. As gestation advances, an increasingly greater proportion of this glucose is partitioned to the gravid uterus. The development of insulin resistance, together with the suppression of pancreatic activity, ensures the preferential uptake of glucose by non-insulin dependent tissues over insulin dependent tissues. These activities favour uterine glucose uptake, decrease adipose glucose uptake, and also promote adipose mobilisation and hepatic gluconeogenesis, so as to meet the increasing energy requirement of pregnancy. It is postulated that through these effects on insulin secretion and associated adipose tissue mobilisation factors, oPL plays a major role in homeorhesis during pregnancy.Doctor of Philosophy (PhD)
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Regnault, Timothy Robert Hume. "Orchestrated partitioning of maternal nutrients during ovine pregnancy." Thesis, View thesis View thesis, 1997. http://handle.uws.edu.au:8081/1959.7/15.
Full textAbstract:
Ovine placental lactogen (oPL) is postulated to be involved in the repartitioning of maternal nutrients during pregnancy, through its effect on insulin metabolism. Ovine pancreatic insulin responses to exogenous glucose are depressed during pregnancy and this depression becomes more pronounced as gestation advances. In addition, under the hormonal environment of rising oPL and growth hormone (oGH) concentrations, maternal whole body glucose irreversible loss (GIL) increases. The percentage of GIL accounted for by uterine glucose uptake also increases with advancing gestation and increasing litter size. Regression analysis of oPL concentration with glucose uterine uptake as a percentage of GIL, accounts for 39% of variation. Maternal oPL concentrations which increase with gestational age, were significantly greater in multiple bearing ewes and ewes subjected to reduced metabolisable energy (ME) intakes. It is postulated that through actions on pancreatic sensitivity, oPL plays a major role as a homeorhetic control during pregnancy. Elevated oPL concentrations were strongly associated with continually depressed pancreatic insulin secretory ability. The reduction in pancreatic sensitivity to glucose was not as a result of elevation in GH or non-esterified fatty acid (NEFA) concentrations. Muscle insulin receptor number and affinity were found to increase with increasing litter size, suggesting that pregnancy associated insulin resistance occurs predominantly in adipose tissue. During ovine pregnancy there is a specific stimulation of maternal gluconeogenesis. As gestation advances, an increasingly greater proportion of this glucose is partitioned to the gravid uterus. The development of insulin resistance, together with the suppression of pancreatic activity, ensures the preferential uptake of glucose by non-insulin dependent tissues over insulin dependent tissues. These activities favour uterine glucose uptake, decrease adipose glucose uptake, and also promote adipose mobilisation and hepatic gluconeogenesis, so as to meet the increasing energy requirement of pregnancy. It is postulated that through these effects on insulin secretion and associated adipose tissue mobilisation factors, oPL plays a major role in homeorhesis during pregnancy.