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PubMedDate not supplied

Plasma glutamine changes after high-intensity exercise in elite male swimmers.

The aim of this study was to establish the pattern and time course of plasma glutamine recovery after acute, high-intensity exercise in well-trained swimmers. In Study 1, elite male swimmers (n=8) performed 15 x 100 m swimming intervals (ITS) at 70% and 95% of maximal 100m freestyle time. Resting plasma glutaminle levels were determined on a nonexercise control day (0% ITS). Venous blood samples were obtained prior to, immediately afte;, and 30, 60, 120, and 150 mini postexercise. In Study 2, the 95% ITS was repeated in elite male swuimmers (n=8), while control subjects (n=8) did not exercise, to test for any diurnal variation in plasma glutamine levels. Venous blood samples were obtained prior to and 2, 4, 6, and 8 h postexercise. In Study 1, no change was observed in plasma glutamine following the 0% (control) and 70% ITS, but following the 95% ITS glutamine decreased significantly (p < 0.01) over the recovery period. In Study 2, plasma glutamine again decreased over the recovery period in the swimmers, but no changes were observed in the controls. It was concluded that intensive swim traininlg results in postexercise decreases in plasma glutamine levels. Because glutamine has been suggested as a marker of overtraining, a need to measure glutaminle at standard times within training programs is indicated.

Adult↗
PubMed1990

Safety of glutamine-enriched parenteral nutrient solutions in humans.

To determine the safety of glutamine-enriched parenteral nutrition, seven normal volunteers were admitted to the Clinical Research Center for three 5-d study periods. The subjects received infusions of parenteral nutrients containing increasing doses of glutamine (0, 0.285, and 0.570 g.kg body wt-1.d-1) substituted for alanine and glycine. Each study period was preceded by greater than or equal to 2 wk of normal food intake. The diets were isocaloric (1.2X estimated basal metabolic rate) and isonitrogenous (1.5 g protein.kg-1.d-1) with nonprotein calories given as dextrose (38%) and fat emulsion (62%). The diets were all well tolerated and there were no untoward effects. Plasma glutamine concentrations increased significantly with glutamine administration but plateaued at concentrations approximately 25% above control values. Ammonia and glutamate, potentially toxic metabolites of glutamine, did not change significantly with glutamine enrichment. Nitrogen balance and hormonal concentrations were unchanged during the three dietary periods. Results of mental-status examinations and continuous performance testing were normal and unchanged throughout the three periods. Glutamine-enriched parenteral nutrient solutions are well tolerated with no associated signs of toxicity in normal humans.

Adult↗
PubMed1995

Increased plasma bicarbonate and growth hormone after an oral glutamine load.

An oral glutamine load was administered to nine healthy subjects to determine the effect on plasma glutamine, bicarbonate, and circulating growth hormone concentrations. Two grams glutamine were dissolved in a cola drink and ingested over a 20-min period 45 min after a light breakfast. Forearm venous blood samples were obtained at zero time and at 30-min intervals for 90 min and compared with time controls obtained 1 wk earlier. Eight of nine subjects responded to the oral glutamine load with an increase in plasma glutamine at 30 and 60 min before returning to the control value at 90 min. Ninety minutes after the glutamine administration load both plasma bicarbonate concentration and circulating plasma growth hormone concentration were elevated. These findings demonstrate that a surprisingly small oral glutamine load is capable of elevating alkaline reserves as well as plasma growth hormone.

Administration, Oral↗
PubMed1997

A prospective randomized study of glutamine-enriched parenteral compared with enteral feeding in postoperative patients.

Plasma amino acids were measured in 17 postoperative subjects randomly assigned to receive for > or = 5 d tube feeding or total parenteral nutrition (TPN) that had identical energy, nitrogen, and glutamine contents. Subjects required gastric or pancreatic surgery for malignancy and were well-matched for age and body mass index. Tube feeding or TPN began on postoperative day 1 and advanced in daily 25% increments to meet goals of 105 kJ . kg body wt-1 . d-1, 1.5 g protein . kg body wt-1 . d-1, and 0.3 g glutamine . kg body wt-1 . d-1. Delivered energy, nitrogen, and glutamine were closely matched on day 4. Nitrogen balance and plasma proteins did not differ significantly between feeding groups. Total indispensable amino acids, branched-chain amino acids, and glutamine declined 25% on postoperative day 1 compared with preoperative day 0. Indispensable and branched-chain amino acid concentrations were restored with 5 d of either tube feeding or TPN. Glutamine concentrations did not differ significantly by feeding group, though a trend suggested that glutamine recovered more slowly in the tube-fed than in the TPN-fed subjects. Plasma amino acids otherwise reflected formula composition with ratios of valine to leucine of 1.24 and 3.69 mumol/L in subjects receiving 5 d of tube feeding or TPN, respectively. These findings suggest that glutamine-enriched tube feeding and TPN can result in similar profiles for most plasma amino acids at carefully matched doses.

Adolescent↗
PubMed2001

Glutamine: the emperor or his clothes?

In this introduction to the Proceedings of the Symposium on Glutamine, we consider various lines of evidence that might potentially lead to an answer to the question posed in the title. We begin with a short summary of the multiple functions of glutamine, which are extensive and, superficially at least, equally as impressive as those of glutamate. However, each of these amino acids may serve an equivalent role in some of these functions due to their ready metabolic interconversion. We raise the question whether glutamine is of primordial or rudimentary significance or whether it is a product of somebody else's existence. Thus, there is a short account of the prebiotic events of evolution that led to the appearance of glutamine and life on Earth. In doing this, it then appears that glutamine is a rather schizophrenic molecule, stable and thermodynamically reliable in biochemical environments, but labile in chemical ones. We then turn to the involvement of glutamine in mammalian N (nitrogen) commerce, with initial emphasis on the nitrogen cycle on Earth, then N transport and N excretion, before assessing its contribution to carbon/energy or C/E commerce. We hypothesize that, in addition to its utilization in immune cell function and in normal intestinal tissues, glutamine is a particularly key anapleurotic and energy-yielding substrate in conditions of hypoxia, anoxia and dysoxia. It also serves as a quantitatively important gluconeogenic metabolite under normal postabsorptive conditions. We postulate that in certain conditions, this carbon-energy econometric function might be by-passed with ornithine. In conclusion, the answer to the question above depends on the context, and this point will receive elaboration in many of the individual contributions that collaborate to form these Proceedings.

Animals↗
PubMed2002

Acute enteral glutamine infusion enhances heme oxygenase-1 expression in human duodenal mucosa.

The heat shock protein, heme oxygenase-1 (HO-1), contributes to the protection of the intestine. Some experimental models suggest that induction of HO-1 by glutamine may contribute to the preservation of intestinal mucosa. The effect of an enteral infusion of glutamine for 6 h on HO-1 expression in duodenal mucosa was studied in healthy men and women and compared with an isonitrogenous mixture of amino acids. After enteral infusion, endoscopic duodenal biopsies were performed and either fixed in formalin for immunohistochemistry or frozen for HO-1 mRNA analysis by reverse transcriptase-polymerase chain reaction. Histologic examination revealed that HO-1 was constitutively expressed in intestinal epithelial cells (IEC), and that glutamine increased the grade of HO-1 immunostaining (P </= 0.01). Glutamine also increased the percentage of HO-1 immunoreactive lamina propria cells (LPC, 10.5 vs. 7.5%, P </= 0.05). Glutamine significantly increased HO-1 mRNA expression compared with control amino acids: median (range) 156 (102-182) vs. 100 (68-179)%, P </= 0.05. The mRNA level for HO-1 was correlated with the percentage of immunoreactive LPC (r = 0.55, P = 0.017) and the grade of immunostaining in IEC (r = 0.51, P = 0.030). In conclusion, glutamine enhanced HO-1 mRNA and protein expression in human duodenal mucosa. These data support further evaluation of the effects of glutamine on intestinal HO-1 during states of intestinal inflammation.

Adult↗
PubMed1993

Glutamine utilization in resting and stimulated platelets.

Exogenous glutamine was metabolized by platelets to glutamate, aspartate, and CO2; whereas no lactate was formed. The amount of aspartate and CO2 produced from glutamine was reduced by the presence of glucose. On the other hand the rate of oxidation of glucose was reduced by the presence of glutamine. The potential energetic value of glutamine was lower than that of glucose, but the amino acid appeared to be a preferential respiratory substrate. The energy provision from glutamine also plays a role in the process of platelet activation, known to require an extra supply of ATP, since thrombin increased the rate of glutamine utilization in platelets. Upon cell activation an increase in aspartate and CO2 formation was observed and the stimulatory effect on glutamine oxidation by thrombin was also maintained in the presence of glucose.

Aspartic Acid↗
PubMed2002

Plasma glutamine and glutamate concentrations in Gabonese children with Plasmodium falciparum infection.

BACKGROUND: Low plasma glutamine levels in critical illness, neonates and burns patients are associated with poor outcome and increased risk of intercurrent infection. AIM: To investigate the relationship between plasma glutamine/glutamate levels and severity/outcome of malaria. DESIGN: Two-hospital prospective study, with both febrile and healthy controls. METHODS: We measured plasma glutamine and glutamate concentrations in 239 Gabonese patients: 145 children with malaria (86 with severe, 36 with moderate and 23 with uncomplicated disease), 42 healthy children, 44 febrile controls and eight healthy adults, and related findings to conventional markers of disease severity such as plasma lactate. RESULTS: Median (IQR) plasma glutamine was lower in uncomplicated falciparum malaria and in moderate malaria than in healthy controls: 353 (287-474) and 379 (293-448) vs. 485 (428-531) micromol/l, respectively; p<0.01 for both malaria groups vs. controls. In contrast, plasma glutamine was within the normal range in those with severe malaria and in febrile control children: 431 (342-525) and 472 (338-547) micromol/l, respectively. Furthermore, plasma glutamine was significantly higher in the children who died with malaria than in survivors: 514 (374-813) (n=12) vs. 399 (316-475) micromol/l (n=133), respectively; p=0.001. There were no significant differences in plasma glutamate concentrations between any of the study groups. DISCUSSION: In severe malaria, there was a positive correlation between plasma glutamine and lactate levels (p=0.009, r=0.281). This correlation may reflect impaired gluconeogenesis. Glutamine supplementation is probably not justified in severe P. falciparum infection.

Biomarkers↗
PubMed1997

Effects of glutamine and taurine on preimplantation development and cleavage of mouse embryos in vitro.

Glutamine and taurine are reported to improve the development of mouse embryos in vitro, and glutamine is a component in CZB and KSOM, media optimized to overcome the 2-cell block in outbred strains of mice. Here we have studied the development of embryos from F1 hybrid female mice in CZB and KSOM, from the zygote to the blastocyst stage, in the presence and absence of 1 mM glutamine and/or 5 mM taurine. Blastocyst formation, rate of development, number of trophectoderm and inner cell mass cells, mitosis, and cell death were examined. Glutamine had no effect on the proportion of embryos developing to the blastocyst stage, but it significantly reduced cell number at the blastocyst stage. The trophectoderm was the lineage most affected, showing increased levels of cell death. Changing the media after 48 h, to remove any possible buildup of toxic metabolites, did not reverse the inhibition by glutamine. Taurine had no effect on blastocyst development of cell number. Development in glutamine-free KSOM (KSOM-Gln) was compared to that in standard CZB and KSOM with glutamine and M16. Early cleavage was slower in M16, but by Day 5 over 84% of embryos had developed to the blastocyst stage in all media, with a similar cell number in M16, CZB, and KSOM. Cell numbers in blastocysts cultured in KSOM-Gln were significantly higher than in the other media and approached those found in vivo.

Animals↗
PubMed1992

Glutamine preserves liver glutathione after lethal hepatic injury.

Glutathione (GSH) is a major antioxidant that protects tissues from free radical injury. Glutamine augments host defenses and may be important in GSH synthesis. Acetaminophen toxicity causes hepatic GSH depletion and hepatic necrosis. The authors hypothesized that glutamine-supplemented nutrition would enhance liver GSH stores and diminish hepatic injury and death after acetaminophen overdose. Wistar rats received either a standard total parenteral nutrition (TPN) solution (STD) or an isocaloric, isonitrogenous glutamine-supplemented solution (GLN). On the 5th day of feeding, animals were given acetaminophen (400 mg/kg intraperitoneally) and then killed at various time points. Standard TPN solution animals had a rapid depletion of hepatic glutathione, whereas GLN animals were resistant to this drop and rapidly repleted hepatic GSH stores. Glutamine-supplemented animals maintained higher plasma glutamine concentrations, had lesser elevations in hepatic enzymes, and sustained significantly fewer complications compared with STD animals. The authors conclude that glutamine-supplemented nutrition preserves hepatic glutathione, protects the liver, and improves survival during acetaminophen toxicity. Glutamine may augment host defenses by enhancing antioxidant protection.

Acetaminophen↗
PubMed1995

Glutamine enhances selectivity of chemotherapy through changes in glutathione metabolism.

OBJECTIVE: Chemotherapy doses are limited by toxicity to normal tissues. Intravenous glutamine protects liver cells from oxidant injury by increasing intracellular glutathione (GSH) content. The authors hypothesized that supplemental oral glutamine (GLN) would increase the therapeutic index of methotrexate (MTX) by improving host tolerance through changes in glutathione metabolism. The authors examined the effects of oral glutamine on tumor and host glutathione metabolism and response to methotrexate. METHODS: Thirty-six 300-g Fischer 344 rats were implanted with fibrosarcomas. On day 21 after implantation, rats were randomized to receive isonitrogenous isocaloric diets containing 1 g/kg/day glutamine or glycine (GLY) by gavage. On day 23 after 2 days of prefeeding, rats were randomized to one of the following four groups receiving an intraperitoneal injection of methotrexate (20 mg/kg) or saline (CON): GLN+MTX, GLY+MTX, GLN-CON, or GLY-CON. On day 24, rats were killed and studied for arterial glutamine concentration, tumor volume, kidney and gut glutaminase activity, and glutathione content (tumor, gut, heart, liver, muscle, kidney, and lung). RESULTS: Provision of the glutamine-enriched diets to rats receiving MTX decreased tumor glutathione (2.38 +/- 0.17 in GLN+MTX vs. 2.92 +/- 0.20 in GLY+MTX, p < 0.05), whereas increasing or maintaining host glutathione stores (in gut, 2.60 +/- 0.28 in GLN+MTX vs. 1.93 +/- 0.18; in GLY+MTX, p < 0.05). Depressed glutathione levels in tumor cells increases susceptibility to chemotherapy. Significantly decreased glutathione content in tumor cells in the GLN+MTX group correlated with enhanced tumor volume loss (-0.8 +/- 1.0 mL in GLN+MTX vs. +9.5 +/- 2.0 mL in GLY+MTX, p < 0.05). CONCLUSION: These data suggest that oral glutamine supplementation will enhance the selectivity of antitumor drugs by protecting normal tissues from and possibly sensitizing tumor cells to chemotherapy treatment-related injury.

Animals↗
PubMed1999

Blood-brain barrier glutamine transport during normoglycemic and hyperglycemic focal cerebral ischemia.

This study examines the effects of middle cerebral artery (MCA) occlusion in the rat on blood to brain glutamine transport, a potential marker of early endothelial cell dysfunction. It also examines whether the effects of ischemia on glutamine transport are exacerbated by hyperglycemia. In pentobarbital-anesthetized rats, 4 hours of MCA occlusion resulted in a marked decline in the influx rate constant for [14C]L-glutamine from 16.1+/-1.2 microL.g(-1).min(-1) in the contralateral hemisphere to 7.3+/-2.5 microL.g(-1).min(-1) in the ischemic core (P < 0.001). This reduction was even greater in xylazine-ketamine-anesthetized rats in which the influx decreased to 2.6+/-1.1 microL.g(-1) min(-1). This greater reduction appears related to the hyperglycemia induced by xylazine-ketamine anesthesia. Glucose injection in pentobarbital-anesthetized rats also resulted in a greater decline in [14C]L-glutamine influx in the ischemic core but had no effect on the contralateral tissue. The effects of hyperglycemia on glutamine transport in the ischemic tissue were associated with a decline in plasma volume, which may reflect either endothelial cell swelling or plugging of the microvasculature. The reduction in glutamine transport during ischemia was progressive, but even as early as 1 hour, there was a 60% and 40% decline in influx in hyperglycemic and normoglycemic rats, respectively. The fall in [14C]L-glutamine influx may reflect a dissipation of the endothelial cell [Na+] gradient. A decline in this gradient would affect many blood-brain barrier transporters with potentially deleterious effects on the ischemic brain.

Animals↗
PubMed1997

Growth hormone and glutamine do not stimulate intestinal adaptation following massive small bowel resection in the rat.

BACKGROUND: Certain nutrients and other trophic factors are highly sensitive stimulants of intestinal adaptation following short bowel syndrome. Growth hormone and glutamine in a modified diet have been shown to enhance nutrient absorption in patients with severe short bowel syndrome. However, neither growth hormone nor glutamine is capable of enhancing adaptation in an animal model. This study was conducted to determine if the combination of glutamine and growth hormone could enhance gut adaptation following massive small bowel resection in the rat. METHODS: Thirty-four male rats received 70% jejunoileal resection. The first group received glycine and rat growth hormone, the second glutamine and rat growth hormone, and the third glycine but no growth hormone. RESULTS: There was no evidence that the combination of glutamine and growth hormone could enhance mucosal mass, mucosal protein, or mucosal DNA levels relative to the other two control groups of animals. Likewise, sucrase activities were not enhanced by glutamine and growth hormone. CONCLUSIONS: It is unlikely that the combination of glutamine and growth hormone will be of benefit in the treatment of patients with short bowel syndrome. The results in previous human studies can be alternatively explained by the long-term nonspecific effect of enteral nutrition on gut adaptation.

Adaptation, Physiological↗
PubMed2004

Effect of glutamine supplementation on diarrhea, interleukin-8 and secretory immunoglobulin A in children with acute diarrhea.

OBJECTIVE: Glutamine is an important fuel for rapidly dividing cells such as enterocytes and lymphocytes. Exogenous glutamine supplementation in catabolic states preserves intestinal mucosal structure and function, decreases bacterial translocation, and supports normal immunologic responses. This study was planned to assess the effect of glutamine supplementation on duration and severity of diarrhea and to assess its immunomodulatory effect by measuring serum interleukin-8 (IL-8) and salivary immunoglobulin A (sIgA) in children with acute diarrhea. METHODS: In this placebo-controlled, double-blind and randomized trial, 6- to 24-month-old otherwise healthy children admitted to the Diarrheal Diseases Training and Treatment Center with acute diarrhea received either 0.3 g/kg/day of glutamine (n = 63) or placebo (n = 65) for 7 days. Serum IL-8 and sIgA levels were determined on admission and 7 days later. All cases were followed until the diarrheal episode ended. Anthropometric measurements and history of subsequent infectious diseases were monitored monthly for 3 months after treatment. RESULTS: Mean duration of diarrhea in the glutamine treated group was significantly shorter than that of the placebo group (3.40 +/- 1.96 days, 4.57 +/- 2.48 days, respectively; P = 0.004). No differences in serum IL-8 and sIgA were found between groups on admission or 1 week later. During 3 month follow-up, mean weight gain and incidence of infectious diseases were similar in both groups. CONCLUSION: Duration of diarrhea was shorter in children supplemented with glutamine. The beneficial impact of glutamine supplementation seems to be through effects on gastrointestinal mucosa rather than the host immune response.

Acute Disease↗
PubMed1996

Impact of enteral feeding of a glutamine-supplemented formula on the hypoaminoacidemic response in trauma patients.

Plasma amino acid concentrations were measured during fasting and after 3 days of enteral feeding in 16 trauma patients on a glutamine-supplemented diet and 14 patients on an isonitrogenous control diet. During fasting, total amino acids, including glutamine, were depressed by 50% and this was attributed to a reduction in both essential and nonessential amino acids. The essential amino acid concentrations increased in both groups after feeding. The nonessential amino acid concentrations also increased in the control group but not in the glutamine group during feeding. Repletion of the glutamine extracellular pool was not evident after an average intake of 27.1 g per day of glutamine for 3 days. Nitrogen balance was similar for the two groups during feeding. We conclude that in this study, enteral glutamine did not increase the glutamine plasma concentration. In addition, both formulas improved the hypoaminoacidemia of essential amino acids but only the control diet improved the nonessential amino acids plasma concentration.

Adolescent↗
PubMed2000

Glutamine and the gastrointestinal tract.

The amino acid glutamine has become one of the most intensively studied nutrients in the field of nutrition and metabolic support. A variety of studies in cell culture systems, animal models of gut mucosal atrophy, injury/repair and adaptation and a limited number of clinical trials demonstrate trophic and cytoprotective effects of glutamine in small bowel and colonic mucosal cells. Although the routine clinical use of glutamine-enriched parenteral and enteral nutrient solutions remains controversial, available data demonstrate both the safety and metabolic and clinical efficacy of glutamine treatment in selected patient groups. Basic investigations are elucidating underlying mechanisms of glutamine action in intestinal cells. These will inform preclinical and clinical investigations designed to determine glutamine efficacy in selected gastrointestinal disorders. Emerging clinical trials will further define the utility of adjunctive glutamine supplementation as a component of specialized nutrition support in gastrointestinal disease.

Adaptation, Biological↗
PubMed2005

Intestinal permeability and systemic infections in critically ill patients: effect of glutamine.

OBJECTIVE: This article provides a critical review of the evidence indicating that an increase in intestinal permeability is associated with the installation of bacteremia, sepsis, and the multiple organ failure syndrome and that glutamine in pharmacologic doses reduces the acute increase of intestinal permeability and the infection frequency in critically ill patients. DATA SOURCE: All studies published until December 2004 about intestinal permeability, bacterial translocation, and glutamine were located by search of PubMed and Web of Science. The reference lists of review articles and primary publications were also examined to identify references not detected in the computer search. STUDY SELECTION: Clinical and experimental studies investigating the correlation between intestinal permeability, bacterial translocation, and frequency of infections, associated or not with the effect of glutamine administration. DATA EXTRACTION: Information regarding patient population, experimental design, glutamine doses and routes of administration, nutritional therapy prescribed, methods used to assess intestinal permeability, metabolic variables, and the frequency of infections were obtained from the primary literature. DATA SYNTHESIS: Intestinal permeability is increased in critically ill patients. The results have not always been consistent, but the studies whose results support the association between intestinal permeability and systemic infections have had better design and more appropriate controls. The administration of glutamine by the intravenous or oral route and at the doses recommended before or immediately after surgery, burns, or the administration of parenteral nutrition has a protective effect that prevents or reduces the intensity of the increase in intestinal permeability. Glutamine reduces the frequency of systemic infections and may also reduce the translocation of intestinal bacteria and toxins, but this has not been demonstrated. CONCLUSIONS: Glutamine administration improves the prognosis of critically ill patients presumably by maintaining the physiologic intestinal barrier and by reducing the frequency of infections.

Bacterial Translocation↗
PubMed2005

Does the addition of glutamine to enteral feeds affect patient mortality?

OBJECTIVE: Studies have failed to consistently demonstrate improved survival in intensive care unit (ICU) patients receiving immune-modulating nutrient-enhanced enteral feeds when compared with standard enteral feeds. The objective was to study in a prospective fashion the effects of adding glutamine to standard or immune-modulated (supplemented with omega-3 fatty acids, beta-carotene, and amino acids such as glutamine and arginine) tube feeds. DESIGN: Prospective, unblinded study using sequential allocation. SETTING: A university surgical trauma ICU. PATIENTS: All surgical and trauma patients admitted to the surgical trauma ICU at a university hospital over a 3-yr period who were to receive enteral feeds (n = 185). INTERVENTIONS: Sequential assignment to three isocaloric, isonitrogenous diets was performed as follows: standard 1-kcal/mL feeds with added protein (group 1), standard feeds with the addition of 20-40 g/day (0.6 g/kg/day) glutamine (group 2), or an immune-modulated formula with similar addition of glutamine (group 3). The goal for all patients was 25-30 kcal/kg/day and 2 g/kg/day protein. MEASUREMENTS AND MAIN RESULTS: Patients were followed until discharge from the hospital. The primary end point was in-hospital mortality, and multiple secondary end points were recorded. In-hospital mortality for group 1 was 6.3% (four of 64) vs. 16.9% (ten of 59, p = .09) for group 2 and 16.1% (ten of 62, p = .09) for group 3. After controlling for age and severity of illness, the difference in mortality between patients receiving standard tube feeds and all patients receiving glutamine was not significant (p < or = .11). There were no statistically significant differences between the groups for secondary end points. CONCLUSIONS: The addition of glutamine to standard enteral feeds or to an immunomodulatory formula did not improve outcomes. These findings suggest that enteral glutamine should not be routinely administered to patients with surgical critical illness.

APACHE↗