THE ROLE OF PLATELET-ACTIVATING FACTOR IN ALTERATIONS OF SYSTEM A AMINO ACID TRANSPORT IN RAT SOLEUS AND EXTENSOR DIGITORUM LONGUS MUSCLES DURING ENDOTOXIC SHOCK

Calorie restriction (CR) decreased placenta and fetal weights in wild-type (wt) and glucose transporter (Glut) 3 heterozygous null (glut3+/−) mice. Because placental nutrient transport is a primary energy determinant of placentofetal growth, we examined key transport systems. Maternal CR reduced intra- and transplacental glucose and leucine transport but enhanced system A amino acid transport in wt mice. These transport perturbations were accompanied by reduced placental Glut3 and leucine amino acid transporter (LAT) family member 2, no change in Glut1 and LAT family member 1, but increased sodium coupled neutral amino acid transporter (SNAT) and SNAT2 expression. We also noted decreased total and active phosphorylated forms of mammalian target of rapamycin, which is the intracellular nutrient sensor, the downstream total P70S6 kinase, and pS6 ribosomal protein with no change in total and phosphorylated 4E-binding protein 1. To determine the role of placental Glut3 in mediating CR-induced placental transport changes, we next investigated the effect of gestational CR in glut3+/− mice. In glut3+/− mice, a key role of placental Glut3 in mediating transplacental and intraplacental glucose transport was established. In addition, reduced Glut3 results in a compensatory increase of leucine and system A transplacental transport. On the other hand, diminished Glut3-mediated intraplacental glucose transport reduced leucine transport and mammalian target of rapamycin and preserved LAT and enhancing SNAT. CR in glut3+/− mice further reduced transplacental glucose transport and enhanced system A amino acid transport, although the increased leucine transport was lost. In addition, increased Glut3 was seen and preserved Glut1, LAT, and SNAT. These placental changes collectively protect survival of wt and glut3+/− fetuses against maternal CR-imposed reduction of macromolecular nutrients.

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Role of estrogen receptor in the regulation of estrogen induced amino acid transport of System A in breast cancer and other receptor positive tumor cells

International Journal of Molecular Medicine ◽

10.3892/ijmm.9.3.271 ◽

2002 ◽

Author(s):

Hari Bhat ◽

Jaydutt Vadgama

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Amino Acid ◽

Tumor Cells ◽

Amino Acid Transport ◽

Acid Transport ◽

System A

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Effect of endotoxic shock on kinetics of system A amino acid transport in rat soleus muscle

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.251.1.r150 ◽

1986 ◽

Vol 251 (1) ◽

pp. R150-R156 ◽

Cited By ~ 1

Author(s):

M. D. Karlstad ◽

M. M. Sayeed

Keyword(s):

Amino Acid ◽

Soleus Muscle ◽

Amino Acid Transport ◽

Endotoxic Shock ◽

Transport Processes ◽

Male Rats ◽

Acid Transport ◽

Amino Acid Transport System ◽

System A ◽

Kinetics Of

This study evaluated the kinetics of system A amino acid transport in soleus muscle during endotoxic shock. Fasted male rats (80-100 g) were killed by decapitation 5 h after the intravenous injection of saline (control) or 20 mg/kg Salmonella enteritidis endotoxin. Soleus muscles (40 mg) from control or endotoxic rats were incubated in oxygenated Krebs-Ringer-bicarbonate buffer (pH 7.4) at 37 degrees C for 20, 40, or 60 min. Initial rates of entry of alpha-aminoisobutyric acid (AIB) into the inulin-inaccessible space of muscles were measured over a wide range of AIB concentrations (0.1-20.0 mM). Initial rates of AIB transport were separated into two parallel transport processes, a saturable carrier-mediated component and a nonsaturable passive diffusive process. The diffusion constant for the nonsaturable process in the endotoxic muscles (0.36 h-1) was 38% greater than control muscles (0.26 h-1). The maximum rate of AIB transport decreased from 55.6 +/- 3.3 nmol . g dry wt-1 . min-1 in controls to 18.3 +/- 1.9 nmol . g dry wt-1 . min-1 in endotoxic muscles. The apparent Km for saturable AIB transport was not different between control (1.68 +/- 0.12 mM) and endotoxic muscles (1.64 +/- 0.19 mM). Alterations of system A amino acid transport in endotoxic soleus muscles were due to an increase in passive AIB diffusion and a decrease in the number and/or activity of existing carriers and not to a change in carrier affinity for AIB. These results elucidate the mechanism for the decreased amino acid transport (system A) by soleus muscle in endotoxic shock.

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Role of Amino Acid Transport System A in the Control of Cell Volume in Cultured Human Fibroblasts

Cellular Physiology and Biochemistry ◽

10.1159/000154601 ◽

1991 ◽

Vol 1 (3) ◽

pp. 131-142 ◽

Cited By ~ 25

Author(s):

Gian C. Gazzola ◽

Valeria Dall’Asta ◽

Franca A. Nucci ◽

Patrizia A. Rossi ◽

Ovidio Bussolati ◽

...

Keyword(s):

Amino Acid ◽

Cell Volume ◽

Transport System ◽

Amino Acid Transport ◽

Human Fibroblasts ◽

Acid Transport ◽

Amino Acid Transport System ◽

System A ◽

Cultured Human Fibroblasts

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Effect of high altitude on human placental amino acid transport

Journal of Applied Physiology ◽

10.1152/japplphysiol.00691.2019 ◽

2020 ◽

Vol 128 (1) ◽

pp. 127-133 ◽

Cited By ~ 2

Author(s):

Owen. R. Vaughan ◽

Fredrick Thompson ◽

Ramón. A. Lorca ◽

Colleen G. Julian ◽

Theresa L. Powell ◽

...

Keyword(s):

Birth Weight ◽

Amino Acid ◽

High Altitude ◽

Sea Level ◽

Amino Acid Transport ◽

Acid Uptake ◽

Acid Transport ◽

Transport Capacity ◽

System A ◽

Low Altitude

Women residing at high altitudes deliver infants of lower birth weight than at sea level. Birth weight correlates with placental system A-mediated amino acid transport capacity, and severe environmental hypoxia reduces system A activity in isolated trophoblast and the mouse placenta. However, the effect of high altitude on human placental amino acid transport remains unknown. We hypothesized that microvillous membrane (MVM) system A and system L amino acid transporter activity is lower in placentas of women living at high altitude compared with low-altitude controls. Placentas were collected at term from healthy pregnant women residing at high altitude (HA; >2,500 m; n = 14) or low altitude (LA; <1,700 m; n = 14) following planned, unlabored cesarean section. Birth weight, but not placenta weight, was 13% lower in HA pregnancies (2.88 ± 0.11 kg) compared with LA (3.30 ± 0.07 kg, P < 0.01). MVM erythropoietin receptor abundance, determined by immunoblot, was greater in HA than in LA placentas, consistent with lower placental oxygen levels at HA. However, there was no effect of altitude on MVM system A or L activity, determined by Na+-dependent [14C]methylaminoisobutyric acid uptake and [3H]leucine uptake, respectively. MVM abundance of glucose transporters (GLUTs) 1 and 4 and basal membrane GLUT4 were also similar in LA and HA placentas. Low birth weights in the neonates of women residing at high altitude are not a consequence of reduced placental amino acid transport capacity. These observations are in general agreement with studies of IUGR babies at low altitude, in which MVM system A activity is downregulated only in growth-restricted babies with significant compromise. NEW & NOTEWORTHY Babies born at high altitude are smaller than at sea level. Birth weight is dependent on growth in utero and, in turn, placental nutrient transport. We determined amino acid transport capacity in placentas collected from women resident at low and high altitude. Altitude did not affect system A amino acid transport across the syncytiotrophoblast microvillous membrane, suggesting that impaired placental amino acid transport does not contribute to reduced birth weight in this high-altitude population.

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