Nutrient Transport

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Thomas Jansson - One of the best experts on this subject based on the ideXlab platform.

  • complex coordinated and highly regulated changes in placental signaling and Nutrient Transport capacity in iugr
    Biochimica et Biophysica Acta, 2020
    Co-Authors: Stephanie Skuby Chassen, Thomas Jansson
    Abstract:

    The most common cause of intrauterine growth restriction (IUGR) in the developed world is placental insufficiency, a concept often used synonymously with reduced utero-placental and umbilical blood flows. However, placental insufficiency and IUGR are associated with complex, coordinated and highly regulated changes in placental signaling and Nutrient Transport including inhibition of insulin and mTOR signaling and down-regulation of specific amino acid Transporters, Na+/K+-ATPase, the Na+/H+-exchanger, folate and lactate Transporters. In contrast, placental glucose Transport capacity is unaltered and Ca2+-ATPase activity and the expression of proteins involved in placental lipid Transport are increased in IUGR. These findings are not entirely consistent with the traditional view that the placenta is dysfunctional in IUGR, but rather suggest that the placenta adapts to reduce fetal growth in response to an inability of the mother to allocate resources to the fetus. This new model has implications for the understanding of the mechanisms underpinning IUGR and for the development of intervention strategies.

  • maternal protein restriction in the rat inhibits placental insulin mtor and stat3 signaling and down regulates placental amino acid Transporters
    Endocrinology, 2011
    Co-Authors: Fredrick J Rosario, Theresa L Powell, Puttur D Prasad, Nina Jansson, Yoshikatsu Kanai, Thomas Jansson
    Abstract:

    Maternal endocrine and metabolic control of placental Nutrient Transport reduces fetal growth in response to protein restriction.

  • il 6 stimulates system a amino acid Transporter activity in trophoblast cells through stat3 and increased expression of snat2
    American Journal of Physiology-cell Physiology, 2009
    Co-Authors: Helen Jones, Thomas Jansson, Theresa L Powell
    Abstract:

    Changes in placental Nutrient Transport are closely associated with abnormal fetal growth. However, the molecular mechanisms underlying the regulation of placental amino acid Transporters are unkno...

  • high fat diet before and during pregnancy causes marked up regulation of placental Nutrient Transport and fetal overgrowth in c57 bl6 mice
    The FASEB Journal, 2009
    Co-Authors: Helen Jones, Theresa L Powell, Laura A Woollett, Nicolette Barbour, Puttur D Prasad, Thomas Jansson
    Abstract:

    Maternal overweight and obesity in pregnancy often result in fetal overgrowth, which increases the risk for the baby to develop metabolic syndrome later in life. However, the mechanisms underlying fetal overgrowth are not established. We developed a mouse model and hypothesized that a maternal high-fat (HF) diet causes up-regulation of placental Nutrient Transport, resulting in fetal overgrowth. C57BL/6J female mice were fed a control (11% energy from fat) or HF (32% energy from fat) diet for 8 wk before mating and throughout gestation and were studied at embryonic day 18.5. The HF diet increased maternal adiposity, as assessed by fat pad weight, and circulating maternal leptin, decreased serum adiponectin concentrations, and caused a marked increase in fetal growth (+43%). The HF diet also increased transplacental Transport of glucose (5-fold) and neutral amino acids (10-fold) in vivo. In microvillous plasma membranes (MVMs) isolated from placentas of HF-fed animals, protein expression of glucose transpo...

  • regulation of placental Nutrient Transport a review
    Placenta, 2007
    Co-Authors: Helen Jones, Theresa L Powell, Thomas Jansson
    Abstract:

    Fetal growth is primarily determined by Nutrient availability, which is intimately related to placental Nutrient Transport. Detailed information on the regulation of placental Nutrient Transporters is therefore critical in order to understand the mechanisms underlying altered fetal growth and fetal programming. After briefly summarizing the cellular mechanisms for placental Transport of glucose, amino acids and free fatty acids, we will discuss factors shown to regulate placental Nutrient Transporters and review the data describing how these factors are altered in pregnancy complications associated with abnormal fetal growth. We propose an integrated model of regulation of placental Nutrient Transport by maternal and placental factors in IUGR.

Theresa L Powell - One of the best experts on this subject based on the ideXlab platform.

  • placental Nutrient Transport in gestational diabetic pregnancies
    Frontiers in Endocrinology, 2017
    Co-Authors: Marisol Castillocastrejon, Theresa L Powell
    Abstract:

    Maternal obesity during pregnancy is rising and is associated with increased risk of developing gestational diabetes mellitus (GDM), defined as glucose intolerance first diagnosed in pregnancy (1). Fetal growth is determined by the maternal Nutrient supply and placental Nutrient transfer capacity. GDM-complicated pregnancies are more likely to be complicated by fetal overgrowth or excess adipose deposition in utero. Infants born from GDM mothers have an increased risk of developing cardiovascular and metabolic disorders later in life. Diverse factors, such as ethnicity, age, fetal sex, clinical treatment for glycemic control, gestational weight gain, and body mass index among others, represent a challenge for studying underlying mechanisms in GDM subjects. Determining the individual roles of glucose intolerance, obesity, and other factors on placental function and fetal growth remains a challenge. This review provides an overview of changes in placental macroNutrient Transport observed in human pregnancies complicated by GDM. Improved knowledge and understanding of the alterations in placenta function that lead to pathological fetal growth will allow for development of new therapeutic interventions and treatments to improve pregnancy outcomes and lifelong health for the mother and her children.

  • regulation of Nutrient Transport across the placenta
    Journal of Pregnancy, 2012
    Co-Authors: Susanne Lager, Theresa L Powell
    Abstract:

    Abnormal fetal growth, both growth restriction and overgrowth, is associated with perinatal complications and an increased risk of metabolic and cardiovascular disease later in life. Fetal growth is dependent on Nutrient availability, which in turn is related to the capacity of the placenta to Transport these Nutrients. The activity of a range of Nutrient Transporters has been reported to be decreased in placentas of growth restricted fetuses, whereas at least some studies indicate that placental Nutrient Transport is upregulated in fetal overgrowth. These findings suggest that changes in placental Nutrient Transport may directly contribute to the development of abnormal fetal growth. Detailed information on the mechanisms by which placental Nutrient Transporters are regulated will therefore help us to better understand how important pregnancy complications develop and may provide a foundation for designing novel intervention strategies. In this paper we will focus on recent studies of regulatory mechanisms that modulate placental Transport of amino acids, fatty acids, and glucose.

  • maternal protein restriction in the rat inhibits placental insulin mtor and stat3 signaling and down regulates placental amino acid Transporters
    Endocrinology, 2011
    Co-Authors: Fredrick J Rosario, Theresa L Powell, Puttur D Prasad, Nina Jansson, Yoshikatsu Kanai, Thomas Jansson
    Abstract:

    Maternal endocrine and metabolic control of placental Nutrient Transport reduces fetal growth in response to protein restriction.

  • il 6 stimulates system a amino acid Transporter activity in trophoblast cells through stat3 and increased expression of snat2
    American Journal of Physiology-cell Physiology, 2009
    Co-Authors: Helen Jones, Thomas Jansson, Theresa L Powell
    Abstract:

    Changes in placental Nutrient Transport are closely associated with abnormal fetal growth. However, the molecular mechanisms underlying the regulation of placental amino acid Transporters are unkno...

  • high fat diet before and during pregnancy causes marked up regulation of placental Nutrient Transport and fetal overgrowth in c57 bl6 mice
    The FASEB Journal, 2009
    Co-Authors: Helen Jones, Theresa L Powell, Laura A Woollett, Nicolette Barbour, Puttur D Prasad, Thomas Jansson
    Abstract:

    Maternal overweight and obesity in pregnancy often result in fetal overgrowth, which increases the risk for the baby to develop metabolic syndrome later in life. However, the mechanisms underlying fetal overgrowth are not established. We developed a mouse model and hypothesized that a maternal high-fat (HF) diet causes up-regulation of placental Nutrient Transport, resulting in fetal overgrowth. C57BL/6J female mice were fed a control (11% energy from fat) or HF (32% energy from fat) diet for 8 wk before mating and throughout gestation and were studied at embryonic day 18.5. The HF diet increased maternal adiposity, as assessed by fat pad weight, and circulating maternal leptin, decreased serum adiponectin concentrations, and caused a marked increase in fetal growth (+43%). The HF diet also increased transplacental Transport of glucose (5-fold) and neutral amino acids (10-fold) in vivo. In microvillous plasma membranes (MVMs) isolated from placentas of HF-fed animals, protein expression of glucose transpo...

Ray B Bryant - One of the best experts on this subject based on the ideXlab platform.

  • role of rainfall intensity and hydrology in Nutrient Transport via surface runoff
    Journal of Environmental Quality, 2006
    Co-Authors: Peter J A Kleinman, M S Srinivasan, Curtis J Dell, John P Schmidt, Andrew N Sharpley, Ray B Bryant
    Abstract:

    Loss of soil Nutrients in runoff accelerates eutrophication of surface waters. This study evaluated P and N in surface runoff in relation to rainfall intensity and hydrology for two soils along a single hillslope. Experimentswereinitiatedon1-by2-mplotsatfoot-slope(6%)andmidslope (30%) positions within an alfalfa (Medicago sativa L.)–orchardgrass (Dactylis glomerata L.) field. Rain simulations (2.9 and 7.0 cm h 21 ) were conducted under wet (spring) and dry (late-summer) conditions. Elevated, antecedent soil moisture at the foot-slope during the spring resulted in less rain required to generate runoff and greater runoff volumes, compared with runoff from the well-drained mid-slope in spring and at both landscape positions in late summer. Phosphorus in runoff was primarily in dissolved reactive form (DRP averaged 71% of totalP),withDRPconcentrationsfromthetwosoilscorrespondingwith soiltestPlevels.Nitrogeninrunoffwasmainlynitrate(NO3–Naveraged 77%oftotalN).Sitehydrology,notchemistry,wasprimarilyresponsible for variations in mass N and P losses with landscape position. Larger runoff volumes from the foot-slope produced higher losses of total P (0.08 kg ha 21 ) and N (1.35 kg ha 21 ) than did runoff from the mid-slope (0.05 total P kg ha 21 ; 0.48 kg N ha 21 ), particularly under wet, spring

  • role of rainfall intensity and hydrology in Nutrient Transport via surface runoff
    Journal of Environmental Quality, 2006
    Co-Authors: Peter J A Kleinman, M S Srinivasan, Curtis J Dell, John P Schmidt, Andrew N Sharpley, Ray B Bryant
    Abstract:

    Loss of soil Nutrients in runoff accelerates eutrophication of surface waters. This study evaluated P and N in surface runoff in relation to rainfall intensity and hydrology for two soils along a single hillslope. Experiments were initiated on 1- by 2-m plots at foot-slope (6%) and mid-slope (30%) positions within an alfalfa (Medicago sativa L.)-orchardgrass (Dactylis glomerata L.) field. Rain simulations (2.9 and 7.0 cm h(-1)) were conducted under wet (spring) and dry (late-summer) conditions. Elevated, antecedent soil moisture at the foot-slope during the spring resulted in less rain required to generate runoff and greater runoff volumes, compared with runoff from the well-drained mid-slope in spring and at both landscape positions in late summer. Phosphorus in runoff was primarily in dissolved reactive form (DRP averaged 71% of total P), with DRP concentrations from the two soils corresponding with soil test P levels. Nitrogen in runoff was mainly nitrate (NO3-N averaged 77% of total N). Site hydrology, not chemistry, was primarily responsible for variations in mass N and P losses with landscape position. Larger runoff volumes from the foot-slope produced higher losses of total P (0.08 kg ha(-1)) and N (1.35 kg ha(-1)) than did runoff from the mid-slope (0.05 total P kg ha(-1); 0.48 kg N ha(-1)), particularly under wet, spring-time conditions. Nutrient losses were significantly greater under the high intensity rainfall due to larger runoff volumes. Results affirm the critical source area concept for both N and P: both Nutrient availability and hydrology in combination control Nutrient loss.

Makoto Taniguchi - One of the best experts on this subject based on the ideXlab platform.

  • Seasonal Changes in Submarine Groundwater Discharge and Associated Nutrient Transport into a Tideless Semi-enclosed Embayment (Obama Bay, Japan)
    Estuaries and Coasts, 2016
    Co-Authors: Ryo Sugimoto, Hisami Honda, Shiho Kobayashi, Yoshitake Takao, Daisuke Tahara, Osamu Tominaga, Makoto Taniguchi
    Abstract:

    We carried out a seasonal study of fresh submarine groundwater discharge (SGD) and associated Nutrient fluxes in a semi-enclosed bay along a tideless coastal zone using a ^222Rn and salinity mass balance model for a whole bay scale. The resulting SGD rates showed large intra-annual variability from 0.05 × 10^6 to 0.77 × 10^6 m^3 day^−1, which were controlled by seasonal changes in the interaction of multiple driving forces, including water table height and seawater level. The highest SGD rate in early spring was induced by heavy snow and low sea level, whereas the seasonal increase in sea level gradually suppressed fresh SGD rates. In summer, an elevated water table may induce higher SGD rates (approximately 0.4 × 10^6 m^3 day^−1) regardless of high sea levels. The highest SGD fraction in total terrestrial freshwater fluxes also occurred in summer (>40 %), due to the decreasing rate of surface river discharge. The seasonally averaged SGD rate was 0.36 × 10^6 m^3 day^−1. This value was similar to the annual groundwater recharge rate (0.33 × 10^6 m^3 day^−1) estimated by the water balance method in the basin. Nutrient fluxes from SGD were approximately 42, 65, and 33 % of all terrestrial fluxes of dissolved inorganic nitrogen, phosphorous, and silicate, respectively. The average fraction of SGD in the water fluxes including terrestrial and oceanic water was low (0.3 %), but that of Nutrient fluxes increased to 20–38 %. Higher Nutrient concentrations in groundwater compensated for the lower volumetric flux of groundwater. Because primary production was mostly restricted by phosphorous throughout the year, phosphorous-enriched Nutrient Transport via SGD would play an important role in biological production.

Mia Niklasson - One of the best experts on this subject based on the ideXlab platform.

  • membrane depolarizing channel blockers induce selective glioma cell death by impairing Nutrient Transport and unfolded protein amino acid responses
    Cancer Research, 2017
    Co-Authors: Mia Niklasson, Gianluca Maddalo, Zuzana Sramkova, Ercan Mutlu, Shimei Wee, Petra Sekyrova, Linnea Schmidt
    Abstract:

    Glioma-initiating cells (GIC) are considered the underlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and undermining the efficacy of conventional chemotherapy. Here we report the discovery that inhibiting T-type voltage-gated Ca2+ and KCa channels can effectively induce selective cell death of GIC and increase host survival in an orthotopic mouse model of human glioma. At present, the precise cellular pathways affected by the drugs affecting these channels are unknown. However, using cell-based assays and integrated proteomics, phosphoproteomics, and transcriptomics analyses, we identified the downstreamsignaling events these drugs affect. Changes in plasma membrane depolarization and elevated intracellular Na+, which compromised Na+-dependent Nutrient Transport, were documented. Deficits in Nutrient deficit acted in turn to trigger the unfolded protein response and the amino acid response, leading ultimately to Nutrient starvation and GIC cell death. Our results suggest new therapeutic targets to attack aggressive gliomas.