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PubMed1993

Direct demonstration by [13C]NMR spectroscopy that glutamine from astrocytes is a precursor for GABA synthesis in neurons.

Primary cultures of cerebral cortical astrocytes and neurons, as well as neurons growing on top of the astrocytes (sandwich co-cultures), were incubated with 1-[13C]glucose or 2-[13C]acetate and in the presence or absence of the glutamine synthetase inhibitor methionine sulfoximine. [13C]NMR spectroscopy at 125 MHz was performed on perchloric acid extracts of the cells or on media collected from the cultures. In addition, the [13C/12C] ratios of the amino acids glutamine, glutamate and 4-aminobutyrate (GABA) were determined by gas chromatography/mass spectroscopy, showing a larger degree of labeling in GABA than in glutamate and glutamine from glucose. Glutamine and glutamate were predominantly labeled from acetate. A picture of cellular metabolism mainly regarding the tricarboxylic acid cycle and glycolysis was obtained. Due to the fact that acetate is not metabolized by neurons to any significant extent, it could be shown that precursors from astrocytes are incorporated into the GABA pool of neurons grown in co-culture with astrocytes. Spectra of media removed from these cultures revealed that likely precursor candidates for GABA were glutamine and citrate. The importance of glutamine is further substantiated by the finding that inhibition of glutamine synthetase, an enzyme present in astrocytes only, significantly decreased the labeling of GABA in co-cultures incubated with 2-[13C]acetate.

Acetates↗

PubMed1976

Ammonia production and pathways of glutamine utilization in rat kidney slices.

Ammonia production from glutamine was studied in slices from non-acidotic and acidotic rat kidneys. Slices from non-acidotic kidneys made 53% as much ammonia from D-glutamine as from L-glutamine during the initial 15 min of incubation. Thereafter the production rate from the L-isomer accelerated while that from the D-isomer remained constant. The accelerated rate of ammonia production from L-glutamine was dependent upon tissue swelling since prevention of swelling reduced the production rate. Swelling activates the mitochondrial glutaminase I pathway as evidenced by the rise in ammonia produced per glutamine utilized ratio as well as by the accelerated rate of CO2 production derived from the oxidative disposal of glutamin's carbon skeleton. Cortical slice swelling activates the mitochondrial pathway in a manner not unlike that seen in vivo during chronic acidosis and may reflect increased permeability to glutamine. Acidotic rat kidneys are not swollen in vivo while cortical slices initially produce 4-fold more ammonia than do non-acidotic slices. After 15 min, this 4-fold difference in total ammonia production drops to only a 2-fold difference due to the swelling-induced activation of the mitochondrial pathway. Consequently, slice swelling obliterates the important fact that ammonia production by the mitochondrial pathway is 15-fold greater in acidotic than in non-acidotic kidneys.

Acidosis↗

PubMed1980

Extracellular matrix metabolism by chondrocytes. 7. Evidence that L-glutamine is an essential amino acid for chondrocytes and other connective tissue cells.

The incorporation of [3H]glycine into acid-insoluble protein and of [3H]acetate into glycosaminoglycans by cultured chick chondrocytes was stimulated by the addition of L-glutamine to the incubation medium. The effect of exogenous L-glutamine on protein synthesis was studied further by examining changes in the sedimentation patterns on sucrose gradients of ribosomes isolated from chondrocytes incubated in presence and absence of L-glutamine. It was found that the absence of L-glutamine caused a disaggregation of polyribosomes that was revered by the addition of this amino acid to the culture medium. No detectable glutamine synthetase activity could be measured in avian articular cartilage. These results indicate that L-glutamine is an essential amino acid for cartilage in that an extracellular supply of this amino acid is required for the maintenance of protein and glycosaminoglycan synthesis. A dependence of L-glutamine was also demonstrated for other avain connective tissues.

Amino Acids, Essential↗

PubMed1986

The simultaneous hydrolysis of glutathione and glutamine by rat kidney gamma-glutamyltransferase.

The simultaneous hydrolysis of L-glutamine and glutathione by rat kidney gamma-glutamyltransferase has been studied. At concentrations of the two substrates giving rates approximating to Vmax, it is shown that glutamine hydrolysis predominates. Under saturating conditions for both substrates, 65% of the glutamic acid produced is derived from glutamine. Using [14C]glutamine it is also shown that at physiological plasma concentrations of glutamine (in excess of 400 microM) and glutathione (20 microM) glutamine hydrolysis is the predominating reaction. We therefore suggest that both glutamine and glutathione are important in vivo donors for gamma-glutamyltransferase.

Animals↗

PubMed1990

Effect of the antiepileptic drug sodium valproate on glutamine and glutamate metabolism in isolated human kidney tubules.

We studied the effects of sodium valproate, a widely used antiepileptic drug and a hyperammonemic agent, on L-[1-14C]glutamine and L-[1-14C]glutamate metabolism in isolated human kidney-cortex tubules. Valproate markedly stimulated glutamine removal as well as the formation of ammonia, 14CO2, pyruvate, lactate and alanine, but it inhibited glucose synthesis; the increase in ammonia formation was explained by a stimulation by valproate mainly of flux through glutaminase (EC 3.5.1.2) and to a much lesser extent of flux through glutamate dehydrogenase (EC 1.4.1.3). By contrast, valproate did not stimulate glutamate removal or ammonia formation, suggesting that the increase in flux through glutamate dehydrogenase observed with glutamine as substrate was secondary to the increase in flux through glutaminase. Accumulation of pyruvate, alanine and lactate in the presence of valproate was less from glutamate than from glutamine. Inhibition by aminooxyacetate of accumulation of alanine from glutamine caused by valproate did not prevent the acceleration of glutamine utilization and the subsequent stimulation of ammonia formation. It is concluded from these data, which are the first concerning the in vitro metabolism of glutamine and glutamate in human kidney-cortex tubules, that the stimulatory effect of valproate is primarily exerted at the level of glutaminase in human renal cortex.

Adult↗

PubMed1995

Glutamine transport and enzymatic activities involved in glutaminolysis in human platelets.

Glutamine is actively metabolized in human platelets, representing a preferential mitochondrial oxidative substrate in these cells. The primary importance of this metabolic route of glutamine is further confirmed here by the observation that platelet glutaminase activity is entirely represented by the phosphate dependent glutaminase or glutaminase I, most probably localized in the mitochondrial platelet fraction and classified by kinetic analysis as a kidney-type form. The following step of the glutamine metabolizing pathway, allowing the entrance of the amino acid skeleton carbons in the Krebs cycle, might be catalyzed by both glutamate dehydrogenase and aspartate transaminase, the first being entirely mitochondrial and the latter 65% mitochondrial. We also investigated platelets for the presence of one or more specific transport systems involved in glutamine uptake and we present the first evidence for two glutamine transport systems in human platelets that by inhibition analysis appear to share characteristics with the Na(+)-dependent ASC system and the Na(+)-independent L system for dipolar amino acid uptake. Both systems display affinity characteristics for glutamine in the range of plasma glutamine concentration and may thus have physiological relevance for the uptake of the amino acid in these cells.

Alanine↗

PubMed1992

Glutamine and glucose metabolism in bovine blood lymphocytes.

1. Glutamine and glucose metabolism was studied in bovine blood lymphocytes incubated at 37 degrees C in the presence of Krebs-Ringer bicarbonate buffer (pH 7.4) containing 1 mM [U-14C]glutamine and 5 mM [U-14C]glucose, respectively. 2. The major metabolic products from glutamine were ammonia, glutamate, and to a lesser extent, aspartate and CO2. Glucose was metabolized mainly to lactate and, to a lesser extent, pyruvate and CO2. These findings indicate incomplete oxidation of glutamine and glucose carbons in bovine blood lymphocytes. 3. Glucose provided three-fold greater amounts of energy to bovine blood lymphocytes than did glutamine on the basis of their measured end-products. Glycolysis accounted for 50% of glucose-derived ATP production. 4. Our findings suggest similar metabolic patterns of glutamine and glucose in lymphocytes between ruminants and non-ruminant species (e.g. rats). However, in contrast to rat peripheral lymphocytes, glucose, rather than glutamine, was a major energy substrate for bovine blood lymphocytes.

Adenosine Triphosphate↗

PubMed1994

Glutamine and glucose metabolism in intraepithelial lymphocytes from pre- and post-weaning pigs.

The metabolism of glutamine (Gln) and glucose was studied in intraepithelial lymphocytes (IEL) from 21-, 29- and 56-day-old pigs. Pigs were weaned at 21 days of age. Cells were incubated at 37 degrees C in the presence of Krebs-Ringer bicarbonate buffer (pH 7.4) containing 1 mM [U-14C]glutamine plus 5 mM glucose, or 5 mM [U-14C]glucose plus 1 mM glutamine. Glucose was converted to lactate, pyruvate and CO2, which accounted for 81, 11 and 8% of measured glucose carbon, respectively. Glutamine was metabolized mainly to glutamate (92% of Gln C) and ammonia, and to a lesser extent, to aspartate (4% of Gln C) and CO2 (4% of Gln C). In the presence of both glucose and glutamine, glucose provided 2-3-fold more ATP to IELs than glutamine in 21-56-day-old pigs, on the basis of their measured end products. The rates of ammonia and glutamate production from glutamine in IELs from 29-day-old pigs were 112 and 90% greater than those in cells from 56-day-old pigs, respectively. The rates of glucose oxidation to CO2 in IELs from 29-day-old pigs were elevated 56 and 64% respectively, compared with 21- and 56-day-old pigs. Elevated rates of substrate metabolism in IELs from 29-day-old post-weaning pigs indicated a metabolic alteration of these cells possibly due to changes in diet and intestinal bacterial population.

Adenosine Triphosphate↗

PubMed2006

The effect of heme oxygenase-1 induction by glutamine on radiation-induced intestinal damage: the effect of heme oxygenase-1 on radiation enteritis.

BACKGROUND: Radiation enteritis is a significant clinical problem in patients receiving ionizing radiation directed at the abdomen or pelvis. The small intestine is the most radiosensitive gastrointestinal organ. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels of the small intestine were measured to determine the oxidative damage caused by radiation. In addition, caspase-3 activity of the small intestine was measured to define the degree of apoptosis. The present study was undertaken to investigate the effect of glutamine administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. METHODS: Rats received 1 g/kg/d glutamine (HO-1-inducer) for 7 days before irradiation and continued for 3 days after irradiation. Zn-prothoporphyin (Zn-PP) 40 micromol/kg was delivered subcutaneously for 1 day before irradiation. Intestinal MPO activities and MDA levels are indicators of oxidative damage, whereas caspase-3 activities show the degree of apoptosis of the small intestine. At histopathologic examination, terminal ileum tissue was analyzed for morphologic changes. Also, the nuclear factor-kappa (NF-kappa) expression level of the terminal ileum was determined with immunohistochemistry methods to show the mucosal inflammatory process. RESULTS: Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels, and HO-1 expression in comparison with the sham group. Glutamine treatment was associated with increased HO-1 expression, decreased MPO activity, caspase-3 activity, and MDA levels. Inhibition of HO-1 activity by Zn-PP completely eliminated the protective effects of glutamine. Histopathologic examination showed that the intestinal mucosal structure was preserved in the glutamine-treated group. In the irradiation group, NF-kappaB overexpression was detected. NF-kappaB positivity was strongest in the intestine of animals in the radiation alone group and the Zn-PP-treated irradiation group. CONCLUSIONS: Glutamine appears to have protective effects against radiation-induced intestinal damage. This protective effect is mediated in part by the induction of HO-1 activity because inhibition of Zn-PP resulted in the complete abolishment of the protective effect of glutamine.

Animals↗

PubMed2004

Glutamine-enriched enteral nutrition increases in vitro interferon-gamma production but does not influence the in vivo specific antibody response to KLH after severe trauma. A prospective, double blind, randomized clinical study.

BACKGROUND & AIMS: Severe trauma leads to an immune suppression, characterized by a Type 2 T-lymphocyte response, contributing to the susceptibility of infectious complications. Plasma concentrations of glutamine (GLN), the preferred fuel for immunocompetent cells, severely decrease after trauma. Since administering glutamine-enriched enteral nutrition (EN) reduces infectious complications in trauma patients, we compared the effect of glutamine-enriched EN with an isocaloric, isonitrogenous enteral control (Con) feeding, on the Type 1 and 2 T-lymphocyte responses. METHODS: Thirty-eight trauma patients (Injury Severity Score >20) were sensitized with Keyhole Limpet Hemocyanin (KLH) within 12 h after trauma (17 GLN group). Healthy volunteers served as controls (HV, n=17). In vitro interferon-gamma (IFN-gamma), IL-4 and IL-10 productions of phytohemagglutinin (PHA)-stimulated PBMCs were determined by ELISA technique. KLH-specific IgG, IgM, IgA, IgG1, IgG2, IgG3, IgG4 and IgE were measured in serum. RESULTS: Both patient groups had a low in vitro (IFN-) production of stimulated PBMCs on d1. On d14, the IFN-gamma production increased significantly in the glutamine group as compared to the controls. IL-4 production was not different between the groups on day 1 (d1). On d14, IL-4 decreased in the control group as compared to the glutamine group. KLH-specific antibodies reached comparable levels in both patients groups and healthy volunteers at d14. CONCLUSIONS: In conclusion, trauma caused a suppressed in vitro cellular immune response presented by a low IFN-gamma production and depressed the IgG and IgM response to KLH directly after trauma. Glutamine increased IFN-gamma production (d14), maintained a normal IL-4 production, but was not acquired for the development of KLH-specific humoral response on d14, in sync suggesting that dietary glutamine supports the restoration of the Type-1 T-lymphocyte responsiveness.

Adjuvants, Immunologic↗

PubMed2006

Effect of glutamine on glutathione kinetics in vivo in dogs.

To determine whether glutamine affects glutathione (GSH, gamma-glutamyl-cysteinyl-glycine) metabolism, seven healthy beagle dogs received 6-h infusions of [(15)N]glutamate and [(13)C]leucine after a 3-day fast. Isotope infusions were performed during oral feeding with an elemental regimen, supplemented with either l-glutamine or an isonitrogenous amino acid mixture, on two separate days and in randomized order. Timed blood samples were obtained, and a surgical duodenal biopsy was performed after 6 h of isotope infusion. GSH fractional synthesis rate (FSR) was assessed from [(15)N]glutamate incorporation into blood and gut GSH, and duodenal protein synthesis from [(13)C]leucine incorporation into gut protein. Glutamine supplementation failed to alter erythrocyte GSH concentration (2189+/-86 vs. 1994+/-102 micromol L(-1) for glutamine vs. control; ns) or FSR (64+/-17% vs. 74+/-20% day(-1); ns). In the duodenum, glutamine supplementation was associated with a 92% rise in reduced/oxidized GSH ratio (P=.024) and with a 44% decline in GSH FSR (96+/-15% day(-1) vs. 170+/-18% day(-1); P=.005), whereas total GSH concentration remained unchanged (808+/-154 vs. 740+/-127 micromol kg(-1); P=.779). We conclude that, in dogs receiving enteral nutrition after a 3-day fast: (1) glutamine availability does not affect blood GSH, and, (2) in contrast, in the duodenum, the preserved GSH pool, along with a decreased synthesis rate, suggests that glutamine may maintain GSH pool and intestinal redox status by acutely decreasing GSH utilization.

Animals↗

PubMed2004

Betaxanthin formation and free amino acids in hairy roots of Beta vulgaris var. lutea depending on nutrient medium and glutamate or glutamine feeding.

Feeding of amino acids to hairy roots of the yellow beet (Beta vulgaris var. lutea) usually results in the formation of the respective betaxanthins. One exception is (S)-glutamate whose feeding leads to an increase in the betaxanthin vulgaxanthin I (glutamine as amino-acid moiety) instead of vulgaxanthin II (glutamate as amino-acid moiety). To elucidate this phenomenon, hairy roots were cultivated in modified standard medium and (S)-glutamate was fed. Under most nutrient conditions tested, glutamine and vulgaxanthin I in the tissue dominated over glutamate and vulgaxanthin II. Glutamate, opposed to glutamine, was readily metabolized so that its concentration was lower than that of glutamine. Maximum concentrations of glutamate were reached when the activity of glutamine synthetase was low. Even then, however, vulgaxanthin II stayed on a low level. In contrast, the level of vulgaxanthin I increased with increasing concentrations of glutamine in the tissue. Also 4-aminobutyric acid (GABA) was a major amino acid in the hairy roots. Its concentration reached maximum levels when (S)-glutamate, a GABA precursor, was fed, or when sucrose, the C source of the roots, was replaced by glucose. The respective GABA-betaxanthin, however, was hardly detectable. When both (S)-glutamate and glucose were supplied, the GABA concentration exceeded that of all other amino acids. Only then the GABA-betaxanthin could be characterized in small amounts. Interestingly, the level of the main betaxanthin, miraxanthin V, consisting of betalamic acid and dopamine, was most markedly reduced by a replacement of sucrose with glucose. We conclude that the reaction of betalamic acid with glutamate and GABA was considerably lower than with glutamine and dopamine, irrespective of the concentration of the amino acid in the tissue. Possible reasons will be discussed, also with respect to the occurrence of species-specific patterns of betaxanthins.

Amino Acids↗

PubMed1997

Hypertonicity induces injury to cultured human endothelium: attenuation by glutamine.

BACKGROUND: Although most preservation solutions as well as some cardioplegic solutions used for organ storage and transplantation are hypertonic, the effects of extracellular hypertonicity on endothelium are not well established. Aims of this study were to evaluate the response of cultured human saphenous vein endothelial cells to extracellular hypertonicity and to investigate the role of the amino acid glutamine in preventing endothelial damage in vitro. METHODS: Eight distinct strains of human saphenous vein endothelial cells were studied. Hypertonic (350 and 400 mosm/kg) media were obtained by supplementing culture medium with sucrose. Cell viability was assessed in the absence or the presence of glutamine through the determination of cell number and protein content of the cultures. Confocal microscopy of cells loaded with the fluorescent dye calcein was also performed. RESULTS: Exposure of human saphenous vein endothelial cells to hypertonic media without glutamine caused significant cell loss within 30 minutes. Cell loss progressed steadily during incubation and after 6 hours reached 50% at 350 mosm/kg and 65% at 400 mosm/kg. In the presence of 2 mmol/L glutamine, endothelial damage was completely prevented at 350 mosm/kg and significantly lessened at 400 mosm/kg compared with glutamine-free media. Confocal microscopy showed that most hypertonicity-treated cells exhibited the typical features of an apoptotic death and confirmed the osmoprotective effect of glutamine. CONCLUSIONS: These results indicate that the supplementation of hypertonic storage solutions with glutamine might exert a partial osmoprotective effect and suggest that the relationship between endothelial damage and tonicity of storage and cardioplegic solutions should be carefully investigated.

Aged↗

PubMed1998

Glutamine improves human preimplantation development in vitro.

OBJECTIVE: To study the effect of glutamine on human preimplantation embryo development in vitro. DESIGN: A randomized, controlled, prospective study of 138 normally fertilized and nontransferred human embryos. On day 2 after fertilization, the embryos were allocated randomly to glucose-free medium with or without 1 mM of glutamine. SETTING: A university hospital-based IVF-ET program. PATIENT(S): Couples undergoing IVF treatment. INTERVENTION(S): Embryo culture. MAIN OUTCOME MEASURE(S): Blastocyst formation, trophectoderm and inner cell mass numbers, and pyruvate uptake and lactate production by individual embryos. RESULT(S): A higher proportion of embryos reached the morula (89% versus 68%, respectively) and blastocyst (71% versus 54%, respectively) stages when cultured with glutamine compared with embryos cultured without glutamine. Blastocyst cell numbers were not statistically significantly different for embryos grown in the presence or absence of glutamine. Pyruvate uptake and lactate production were higher in the presence of glutamine throughout development; these increases were statistically significant at the blastocyst stage. CONCLUSION(S): This study demonstrates that supplementation of the culture medium with glutamine is beneficial for human preimplantation embryo development in vitro, increasing the proportion of embryos that develop to the morula and blastocyst stages.

Blastocyst↗

PubMedDate not supplied

Plasma glutamine levels and falciparum malaria.

Glutamine deficiency is associated with increased rates of sepsis and mortality, which can be prevented by glutamine supplementation. Changes in glutamine concentration were examined in Ghanaian children with acute falciparum malaria and control cases. The mean (SD) plasma glutamine concentration was lower in patients with acute malaria (401 (82) mumol/L, n = 50) than in control patients (623 (67) mumol/L, n = 7; P < 0.001). Plasma glutamine concentrations all rose in convalescence. The mean (SD) increase in plasma glutamine was 202 (123) mumol/L (n = 18; P < 0.001) compared with acute infection. We conclude that acute falciparum malaria is associated with large decreases in plasma glutamine and these falls may increase susceptibility to sepsis and dyserythropoeisis.

Case-Control Studies↗

PubMed1997

Effect of glutamine-enriched total parenteral nutrition on small intestinal gut-associated lymphoid tissue and upper respiratory tract immunity.

BACKGROUND: Our prior work shows that total parenteral nutrition (TPN) causes small intestinal gut-associated lymphoid tissue (GALT) atrophy, lowers small intestinal immunoglobulin A (IgA) levels, and impairs secretory IgA-mediated mucosal immunity of the upper respiratory tract. These experiments examine whether an isonitrogenous 2% glutamine-enriched TPN solution prevents these changes. METHODS: Institute of Cancer Research mice were randomized to chow (chow), intravenous feeding of a TPN solution (TPN), or glutamine-enriched TPN (glutamine) groups. After mice were fed for 5 days, lymphocytes were isolated from Peyer's patches, the intraepithelial layer, and lamina propria to determine cell yields and phenotypes. Total small intestinal IgA levels were analyzed by means of enzyme-linked immunosorbent assay. In a second series of experiments, mice underwent intranasal inoculation with H1N1 virus to establish immunity. After 3 weeks mice were randomized to chow, TPN, or glutamine groups. After feeding for 5 days, mice were rechallenged with intranasal virus and killed at 40 hours to determine viral shedding from the upper respiratory tract. RESULTS: Total lymphocyte yield in the Peyer's patches, the intraepithelial layer, and lamina propria, small intestinal IgA levels, and the CD4+/CD8+ ratio in the lamina propria decreased with TPN but remained normal with glutamine. On rechallenge, 87% of the mice in the TPN group shed virus in nasal secretions, whereas only 38% of the glutamine-treated group (p < 0.05 versus TPN) and 7.1% of the chow group (p < 0.002 versus TPN) were virus positive. CONCLUSIONS: Isonitrogenous supplementation of TPN with 2% glutamine improves IgA-mediated protection in the upper respiratory tract and normalizes GALT populations.

Animals↗

PubMed1994

Muscle ammonia and glutamine exchange during chronic liver insufficiency in the rat.

The aim of this study was to investigate the role of skeletal muscle in ammonia and glutamine metabolism during chronic hyperammonemia induced by liver insufficiency. The hindquarter ammonia and amino acid fluxes and muscle tissue concentrations were studied in two rat models of chronic liver insufficiency, portacaval shunting and portacaval shunting plus bile-duct ligation, as well as in sham-operated animals, 7 and 14 days after surgery, and in normal, unoperated rats. To reduce nutritional influences, portacaval-shunted rats and sham-operated rats were pair-fed to portacaval shunt biliary obstruction rats. Arterial ammonia levels were elevated in both liver insufficiency groups. In the portacaval shunting plus bile-duct ligation group, arterial glutamine levels were elevated compared with sham-operated controls. No net hind-quarter ammonia uptake was observed in any of the groups, despite hyperammonemia in the chronic liver insufficiency groups. Hindquarter glutamine release was always increased in the liver insufficiency groups compared with sham-operated controls, despite similar muscle glutamine levels in the sham-operated and hyperammonemic groups, suggesting enhanced muscle glutamine synthesis in the latter groups. Muscle ammonia levels were always increased and muscle glutamate decreased in the hyperammonemic groups, probably indicating glutamate consumption by enhanced glutamine synthesis. The increased phenylalanine tissue concentrations and efflux in portacaval shunt/biliary obstruction rats suggest that enhanced net muscle protein breakdown, amino acid catabolism and transamination, rather than ammonia uptake from the blood furnish amino acids and ammonia for enhanced glutamine synthesis. These experiments suggest that nutritional factors are important in explaining altered muscle metabolism during chronic liver insufficiency.

Amino Acids↗

PubMedDate not supplied

Glutamine transport at the blood-brain and blood-cerebrospinal fluid barriers.

Glutamine has multiple physiological and pathophysiological roles in the brain. Because of their position at the interface between blood and brain, the cerebral capillaries and the choroid plexuses that form the blood-brain barriers (BBB) and blood-cerebrospinal fluid (CSF) barriers, have the potential to influence brain glutamine concentrations. Despite this, there has been a paucity of data on the mechanisms and polarity of glutamine transport at these barrier tissues. In situ brain perfusion in the rat, indicates that blood to brain L-[14C]glutamine transport at the blood-brain barrier is primarily mediated by a pH-dependent, Na(+)-dependent, System N transporter, but that blood to choroid plexus transport is primarily via a pH-independent System N transporter and a Na(+)-independent carrier that is not System L. Transport studies in isolated rat choroid plexuses and primary cultures of choroid plexus epithelial cells indicate that epithelial L-[14C]glutamine transport is polarized (apical uptake>basolateral) and that uptake at the apical membrane is mediated by pH dependent System N transporters (identified as SN1 and SN2 by polymerase chain reaction) and the Na(+)-independent System L. Blood-brain barrier System N transport is markedly effected by cerebral ischemia and may be a good marker of endothelial cell dysfunction. The multiple glutamine transporters at the blood-brain and blood-CSF barriers may have role in meeting the metabolic needs of the brain and the barrier tissues themselves. However, it is likely that the main role of these transporters is removing glutamine, and thus nitrogen, from the brain.

Animals↗