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PubMed1972

Metabolism of glutamine by the intact functioning kidney of the dog. Studies in metabolic acidosis and alkalosis.

The renal conversion of glutamine to glucose and its oxidation to CO(2) were compared in dogs in chronic metabolic acidosis and alkalosis. These studies were performed at normal endogenous levels of glutamine utilizing glutamine-(34)C (uniformly labeled) as a tracer. It was observed in five experiments in acidosis that mean renal extraction of glutamine by one kidney amounted to 27.7 mumoles/min. Of this quantity, 5.34 mumoles/min was converted to glucose, and 17.5 mumoles/min was oxidized to CO(2). Acidotic animals excreted an average of 41 mumoles/min of ammonia in the urine formed by one kidney. In contrast, in five experiments in alkalosis, mean renal extraction of glutamine amounted to 8.04 mumoles/min. Of this quantity, 0.92 mumole/min was converted to glucose, and 4.99 mumoles/min was oxidized to CO(2). Alkalotic animals excreted an average of 3.23 mumoles/min of ammonia in the urine. We conclude that renal gluconeogenesis is not rate limiting for the production and excretion of ammonia in either acidosis or alkalosis. Since 40% of total CO(2) production is derived from oxidation of glutamine by the acidotic kidney and 14% by the alkalotic kidney, it is apparent that renal energy sources change with acid-base state and that glutamine constitutes a major metabolic fuel in acidosis.

Acid-Base Equilibrium↗
PubMedDate not supplied

Effect of alanyl-glutamine on leucine and protein metabolism in endotoxemic rats.

BACKGROUND: Branched-chain amino acids (BCAA; valine, leucine, and isoleucine) have a regulatory effect on protein metabolism and are the main donor for synthesis of alanine and glutamine in the skeletal muscle. This study was performed to investigate whether exogenous alanine or glutamine would affect leucine and protein metabolism in intact and endotoxemic rats. METHODS: Rats were injected with endotoxin of Salmonella enteritidis or saline. Thirty minutes later, the effects of endotoxemia and L-alanyl-L-glutamine (AG) on leucine and protein metabolism were evaluated using a primed constant infusion of [1-14C]leucine, endotoxin, and AG (200 mg/mL) solution or an infusion of [1-14C]leucine without endotoxin or AG. The specificity of the effect of exogenous alanine and glutamine was evaluated by a single infusion of alanine, glutamine, and glycine in a separate study. RESULTS: Endotoxin treatment induced more negative net protein balance caused mainly by an increase in whole-body proteolysis. Protein synthesis increased in kidneys, colon, and spleen, while a decrease was observed in skeletal muscle. The impressive effects of AG were the decrease in plasma branched-chain amino acid (BCAA) levels, decrease in leucine oxidized fraction, and improvement of protein balance associated with a decrease in whole-body proteolysis. Similar changes in leucine and protein metabolism were induced by infusion of alanine or glutamine but not by infusion of glycine. CONCLUSIONS: IV administration of alanine or glutamine improves protein balance and decreases leucine oxidized fraction in postabsorptive state and in endotoxemia. Decreased proteolysis is the main cause of decreased plasma BCAA levels after AG treatment.

Alanine↗
PubMedDate not supplied

Effect of glutamine on phagocytosis and bacterial killing by normal and pediatric burn patient neutrophils.

Glutamine is essential for the function of lymphocytes and macrophages, where it serves, among other things, as a source of energy. Little information is available concerning the fuel that polymorphonuclear cells use for their metabolic and bactericidal functions. It was the purpose of this study to determine whether glutamine would enhance the in vitro bactericidal function of normal neutrophils and whether the amino acid would restore the observed impaired function in burn patients to or above the normal level. Twelve burn patients with total body surface area burns ranging from 32% to 87% were studied. At various postburn times, neutrophils were isolated and their ability to kill Staphylococcus aureus in the presence and absence of glutamine was determined and compared with that in normal subjects. Glutamine enhanced the bactericidal function of normal neutrophils. In every patient, at all but two postburn times, glutamine caused an improvement in the observed abnormal neutrophil bactericidal function and often restored it to or slightly above the normal level. Glutamine had no effect on the expression of C3b receptors (CR1 or CD35) or on phagocytosis by the cells. This study confirms the beneficial effects of glutamine in at least one arm of the immune system and adds evidence for the possible advantage of including this amino acid in the diets of burn and other trauma patients.

Adolescent↗
PubMedDate not supplied

The effect of enteral glutamine deprivation and supplementation on the structure of rat small-intestine mucosa during a systemic injury response.

BACKGROUND: An aseptic model of tissue injury (the induction of abscesses by subcutaneous injections of turpentine) was used to examine the proposal that changes in glutamine metabolism lead to structural damage in the epithelium of the small intestine during the systemic response to injury and to investigate the role of dietary glutamine in the maintenance of mucosal structure in the small intestine of control and injured rats. METHODS: Glutamine-free and glutamine-rich (3.6% glutamine by weight) diets were fed to rats before and during an acute-phase response to injury. Pair-fed groups of animals enabled an independent assessment to be made of the effects of the associated dietary restriction on the mucosal epithelium. RESULTS: Adaptive increases in villus height and crypt depth were seen in response to 4 days of feeding of the glutamine diet. Pair-feeding (30% dietary restriction) of either diet induced mucosal atrophy (loss of wet weight and nitrogen) without changes in villus height or crypt depth in the proximal tercile of the small intestine. Systemic injury, however, had no effect on the weight or nitrogen content of the mucosa (relative to pair-feeding). Gross histologic appearance, villus height, and crypt depth were also unchanged by the response to injury. CONCLUSIONS: The study provided no evidence to support the proposal that alterations in the availability of dietary glutamine during systemic injury (induced by turpentine injections) lead to structural damage to the epithelium.

Animals↗
PubMedDate not supplied

Glutamine dipeptide-supplemented parenteral nutrition reverses gut atrophy, disaccharidase enzyme activity, and absorption in rats.

BACKGROUND: Total parenteral nutrition (TPN) is associated with intestinal atrophy and dysfunction possibly attributed to the absence of the nonessential amino acid glutamine from commercially available TPN solutions because of the instability of the monoamino acid during heat sterilization and storage. The use of stable dipeptides may overcome this problem. In this study we tested the hypothesis that glutamine dipeptide supplementation with alanyl-L-glutamine during TPN for 10 days would reverse small bowel atrophy and TPN-induced dysfunction in rats. METHODS: A conventional TPN solution (250 kcal/kg bw) was compared with an isocaloric and isonitrogenous TPN supplemented with alanyl-L-glutamine dipeptide. A food-fed control group was included (n = 6 each group). Jejunum mucosal architecture, absorption of water and glucose, and disaccharidase activity of maltase and alkaline phosphatase were evaluated. RESULTS: TPN-induced villous atrophy, significantly reduced absorption rate, and decreased activity of villous enzymes, compared with the TPN group, could be reversed by supplementation of glutamine dipeptide alanyl-L-glutamine to parenteral nutrition solutions with no difference to the control group. CONCLUSIONS: Glutamine dipeptide-enriched parenteral nutrition preserves mucosal structure and reversed atrophy-associated dysfunction.

Alkaline Phosphatase↗
PubMedDate not supplied

Effect of long-term oral glutamine supplements on small intestinal permeability in patients with Crohn's disease.

BACKGROUND: Glutamine is a major fuel and an important nitrogen source for the small intestinal cell. It plays a key role in maintaining mucosal cell integrity and gut barrier function. Increased permeability may be a factor in the pathogenesis of Crohn's disease and may be an interesting parameter in the follow-up of the disease. Therefore, the aim of this study was to examine whether oral glutamine supplements are able to restore an increased intestinal permeability in patients with Crohn's disease. METHODS: The inclusion criteria for the study were Crohn's disease and a disturbed small intestinal permeability for 51Cr-EDTA. Of 38 patients screened, 18 had an increased permeability (6 hours urinary excretion >1.1% of label recovered in urine). Fourteen patients were included in the study and were randomized to receive either oral glutamine (7 g three times per day; n = 7) or placebo (7 g glycine three times per day; n = 7) in addition to their normal treatment during a 4-week period. The study was performed in a double-blind manner. RESULTS: Baseline permeability (mean +/- SD) was 2.32%+/-0.77% dose in the glutamine group and 2.29%+/-0.67% dose in the placebo group. Permeability did not change significantly after glutamine (3.26%+/-2.15% dose) or after placebo (2.27%+/-1.32% dose). There was no significant effect on plasma glutamine, plasma glutamate, plasma ammonium, Crohn's disease activity index, C-reactive protein, or nutritional status. CONCLUSIONS: Oral glutamine supplements, in the dose administered, do not seem to restore impaired permeability in patients with Crohn's disease.

Administration, Oral↗
PubMedDate not supplied

Glutamine: indicated in cancer care?

Glutamine is a nonessential amino acid contained in most dietary proteins and provides immune functions and fuel for the small intestine. For healthy people, dietary glutamine (from protein) usually is considered adequate. Results of research evaluating the potential benefits of glutamine during cancer therapy are encouraging but remain inconclusive. Some researchers have suggested recently that glutamine may, in fact, be a conditionally essential amino acid (Buchman, 2001). Decreases in glutamine levels after trauma or major burns, postoperatively, and in patients with diseases such as inflammatory bowel disease, AIDS, and cancer are widely recognized and acknowledged (Medina, 2001; Miller, 1999). The interpretation of data suggesting that glutamine supplementation is of benefit in almost any clinical situation is controversial. Additional research is needed to confirm the mechanism of action and efficacy of glutamine as adjuvant therapy in patients receiving cancer treatment.

Chemotherapy, Adjuvant↗
PubMed1994

Glutamine metabolism in children with short-bowel syndrome: a stable isotope study.

Because glutamine is thought to be a major fuel for developing gut, we tested the hypothesis that extensive small-bowel resection alters whole-body glutamine metabolism in vivo. Eleven infants and children who had undergone extensive small intestinal resection (residual bowel length: 35 +/- 13 cm; mean +/- SD) and four control infants received 4-h primed, continuous i.v. infusions of L-[(1-13C]leucine and L-[2-15N]glutamine in the postabsorptive state. The appearance rates of glutamine and leucine into plasma were determined from stable isotope enrichments in plasma at steady state. We observed the following: 1) Regardless of intestinal status, leucine and glutamine fluxes were higher in infants than values previously reported for adults. 2) Small-bowel resection was associated with a reduction in glutamine appearance rate (568 +/- 124 mumol.kg lean body mass-1.h-1 in short-bowel syndrome infants versus 816 +/- 149 mumol.kg lean body mass-1.h-1 in control infants; p < 0.05). 3) In contrast, leucine appearance rate was unaltered in short-bowel syndrome patients. The findings suggest that the small intestine plays a prominent role in glutamine metabolism in human infants.

Adult↗
PubMed2005

Amino acids, glutamine, and protein metabolism in very low birth weight infants.

Glutamine has been proposed to be conditionally essential for premature infants, and the currently used parenteral nutrient mixtures do not contain glutamine. De novo glutamine synthesis (DGln) is linked to inflow of carbon into and out of the tricarboxylic acid (TCA) cycle. We hypothesized that a higher supply of parenteral amino acids by increasing the influx of amino acid carbon into the TCA cycle will enhance the rate of DGln. Very low birth weight infants were randomized to receive parenteral amino acids either 1.5 g/kg/d for 20 h followed by 3.0 g/kg/d for 5 h (AA1.5) or 3.0 g/kg/d for 20 h followed by 1.5 g/kg/d for 5 h (AA3.0). A third group of babies received amino acids 1.5 g/kg/d for 20 h followed by 3.0 g/kg/d for 20 h (AA-Ext). Glutamine and protein/nitrogen kinetics were examined using [5-(15)N]glutamine, [2H5]phenylalanine, [1-(13)C,15N]leucine, and [15N2]urea tracers. An acute increase in parenteral amino acid infusion for 5 h (AA1.5) resulted in decrease in rate of appearance (Ra) of phenylalanine and urea, but had no effect on glutamine Ra. Infusion of amino acids at 3.0 g/kg/d for 20 h resulted in increase in DGln, leucine transamination, and urea synthesis, but had no effect on Ra phenylalanine (AA-Ext). These data show an acute increase in parenteral amino acid-suppressed proteolysis, however, such an effect was not seen when amino acids were infused for 20 h and resulted in an increase in glutamine synthesis.

Amino Acids↗
PubMed1995

Quantitative analysis of metamorphosis induced by L-glutamine in embryos of the sea urchin, Hemicentrotus pulcherrimus.

Metamorphosis of the sea urchin, Hemicentrotus pulcherrimus, can be induced by L-glutamine as reported previously for Pseudocentrotus depressus [15]. To analyze more precisely the process of metamorphosis induced by L-glutamine, the development of the echinus rudiment (ER) was classified into six stages. The stage at which the larvae underwent the normal metamorphosis by glutamine treatment was confirmed. The time of the glutamine treatment required for metamorphosis (the eversion of ER) was over 10 hr but treatment for more than 25 hr tended to decrease the number of metamorphosed larvae, although the larval arms had mostly been resorbed. The time of glutamine treatment to induce the metamorphosis, depended on the development of ER; more time was required for the younger larvae and less time for the older. The high mitotic activities observed in the cells of the ciliary bands were markedly decreased in the glutamine-treated larvae to metamorphose. These findings suggested that a degenerative process of metamorphosis including cell death is induced by L-glutamine.

Animals↗
PubMed2003

Glutamine supplementation in vitro and in vivo, in exercise and in immunodepression.

In situations of stress, such as clinical trauma, starvation or prolonged, strenuous exercise, the concentration of glutamine in the blood is decreased, often substantially. In endurance athletes this decrease occurs concomitantly with relatively transient immunodepression. Glutamine is used as a fuel by some cells of the immune system. Provision of glutamine or a glutamine precursor, such as branched chain amino acids, has been seen to have a beneficial effect on gut function, on morbidity and mortality, and on some aspects of immune cell function in clinical studies. It has also been seen to decrease the self-reported incidence of illness in endurance athletes. So far, there is no firm evidence as to precisely which aspect of the immune system is affected by glutamine feeding during the transient immunodepression that occurs after prolonged, strenuous exercise. However, there is increasing evidence that neutrophils may be implicated. Other aspects of glutamine and glutamine supplementation are also addressed.

Clinical Trials as Topic↗
PubMed1988

Glutamine and ammonium handling by anaesthetized rats.

The infusion of ether anesthaetized rats with 0.2 M (1 mmols in total) ammonium acetate or glutamine were compared with the infusion of 0.2 M NaCl. The levels of circulating glucose, amino acids, lactate, urea and ammonium were measured as well as liver glycogen and tissue amino acids and the liver and muscle activities of carbamoyl phosphate synthetases I and II, glutamate dehydrogenase, glutamine synthetase and adenylate deaminase. Neither treatment altered the glucose and glycogen homeostasis. The infusion of ammonium did not result in increases in circulating ammonium, but resulted in increased circulating urea after a short delay; the infusion of glutamine resulted also in urea production but much later on. Glutamine infusion also resulted in increased tissue free amino-acid levels. There was little alteration in enzyme activities, except for decreased glutamine synthetase and adenylate deaminase activity in muscle of glutamine-infused rats and higher tissue carbamoyl phosphate synthetase II. The results agree with a fast removal of infused ammonium, and maintenance of glutamine, with their channeling towards urea production at a rate comparable with that of infusion, that did not alter significantly the homeostasis of the experimental animals.

AMP Deaminase↗
PubMed1995

Depression of plasma glutamine concentration after exercise stress and its possible influence on the immune system.

OBJECTIVE: To determine whether plasma glutamine levels can be used as an indicator of exercise-induced stress, and to consider the possible effects of low plasma glutamine concentrations on the immune system. METHODS: We used two exercise regimens: in Trial 1 seven male subjects were randomly stressed on a treadmill at 0, 30%, 60%, 90% and 120% of their maximal oxygen uptake (VO2max); in Trial 2 five highly trained male subjects underwent intensive interval training sessions twice daily for ten days, followed by a six-day recovery period. RESULTS: Plasma glutamine concentrations decreased significantly from an average of 1244 +/- 121 mumol/L to 702 +/- 101 mumol/L after acute exercise at 90% VO2max (P < 0.05) and to 560 +/- 79 mumol/L at 120% VO2max (P < 0.001). Four of the five subjects showed reduced plasma glutamine concentrations by Day 6 of the overload training trial, with all subjects displaying significantly lower glutamine levels by Day 11. However, glutamine levels showed a variable rate of recovery over the six-day recovery period, with two subjects' levels remaining low by Day 16. CONCLUSIONS: Reduced plasma glutamine concentrations may provide a good indication of severe exercise stress.

Exercise↗
PubMed1992

Clinical and metabolic efficacy of glutamine-supplemented parenteral nutrition after bone marrow transplantation. A randomized, double-blind, controlled study.

OBJECTIVE: To determine whether glutamine-supplemented parenteral nutrition improves nitrogen retention and reduces hospital morbidity compared with standard parenteral nutrition after bone marrow transplantation. DESIGN: Double-blind, randomized, controlled clinical trial. SETTING: University teaching hospital. PATIENTS: Forty-five adults receiving allogeneic bone marrow transplants for hematologic malignancies. INTERVENTION: Parenteral nutrition was initiated the day after bone marrow transplantation (day 1). The experimental solution was supplemented with L-glutamine (0.57 g/kg body weight per day) and provided estimated requirements for energy and protein. The control solution was a standard, glutamine-free, isonitrogenous, isocaloric formula. MEASUREMENTS: Nitrogen balance was determined between days 4 and 11 in the initial 23 patients. The incidence of clinical infection and microbial colonization, time until bone marrow engraftment, indices of clinical care, and other data related to hospital morbidity were recorded for all patients. RESULTS: The glutamine-supplemented patients (n = 24) were clinically similar to the controls (n = 21) at entry. Nutrient intake was similar in both groups; however, nitrogen balance was improved in the glutamine-supplemented patients relative to the controls (-1.4 +/- 0.5 g/d compared with -4.2 +/- 1.2; P = 0.002). Fewer experimental patients developed clinical infection (three compared with nine in the control group; P = 0.041), and the incidence of microbial colonization was also significantly reduced. Hospital stay was shortened in patients receiving glutamine supplementation (29 +/- 1 d compared with 36 +/- 2 d; P = 0.017). CONCLUSION: Patients receiving glutamine-supplemented parenteral nutrition after bone marrow transplantation had improved nitrogen balance, a diminished incidence of clinical infection, lower rates of microbial colonization, and shortened hospital stay compared with patients receiving standard parenteral nutrition. These effects occurred despite no differences between groups in the incidence of fever, antibiotic requirements, or time to neutrophil engraftment.

Adult↗
PubMed1999

Effects of adrenaline on glucose and glutamine metabolism and superoxide production by rat neutrophils.

Despite the large body of information on the role of corticosteroids in regulating lymphocyte and phagocyte function, the role of the hormone adrenaline in immunoregulation is an under-investigated topic. The present study has addressed the effects of adrenaline on the rates of utilization and oxidation of glucose and glutamine, the phagocytic capacity and the rate of superoxide production by rat neutrophils. Incubation of rat neutrophils in the presence of 50 microM adrenaline caused a marked elevation in glucose metabolism, an effect that could be blocked by propranolol. Adrenaline caused a partial inhibition of glutamine utilization by neutrophils, an effect that was also blocked by propranolol. These effects of adrenaline could be mimicked by 100 microM dibutyryl cAMP. Phosphate-dependent glutaminase activity was significantly elevated in neutrophils incubated in the presence of 50 microM adrenaline or 100 microM dibutyryl cAMP for 1 h, whereas glutamine oxidation was significantly depressed (P<0.05) under these conditions. The elevation in enzyme activity was only partially blocked by propranolol. The phagocytic activity of rat neutrophils was not altered by adrenaline in the presence of either glucose or glutamine. The rate of phorbol 12-myristate 13-acetate-induced superoxide production in the presence of glucose was potently reduced by the addition of 5 nM or 50 microM adrenaline. This effect could be mimicked by dibutyryl cAMP. However, when rat neutrophils were incubated in the presence of glutamine plus adrenaline (5 nM or 50 microM), the rate of superoxide production was only marginally reduced. These findings support the proposition that adrenaline may deviate the flux of glucose from the NADPH-producing pentose phosphate pathway, thus reducing substrate availability for the superoxide-generating NADPH oxidase. However, glutamine metabolism may still give rise to substantial quantities of NADPH from the glutaminolysis pathway. We postulate that glutamine metabolism may thus provide a protective mechanism against the inhibitory effect of adrenaline on superoxide production by neutrophils.

Adrenergic beta-Agonists↗
PubMed1999

Effect of glutamine limitation on the death of attached Chinese hamster ovary cells.

The effect of glutamine depletion on the death of attached Chinese hamster ovary (CHO) cells was investigated. Experiments were performed using an anchorage dependent CHO cell line expressing gamma-IFN and a second cell line obtained by transfection of that cell line with the human bcl-2 (hbcl-2). Either cell line could grow in media devoid of glutamine with minimal cell death due to endogenous glutamine synthetase activity that allowed cells to synthesize glutamine from glutamic acid in the medium. However, compared to control cultures in glutamine-containing media, the cell growth rate in glutamine-free media was slower with an increased fraction of cells distributed in the G0/G1 phase. The slower rate of cell cycling apparently protected the cells from entering apoptosis when they were stimulated to proliferate in an environment devoid of other protective factors, such as serum or over-expressed hbcl-2. The depletion of both glutamine and glutamic acid did cause cell death, which could be mitigated by hbcl-2 over-expression.

Animals↗
PubMed1999

Therapeutic considerations of L-glutamine: a review of the literature.

The most abundant amino acid in the bloodstream, L-glutamine fulfills a number of biochemical needs. It operates as a nitrogen shuttle, taking up excess ammonia and forming urea. It can contribute to the production of other amino acids, glucose, nucleotides, protein, and glutathione. Glutamine is primarily formed and stored in skeletal muscle and lungs, and is the principal metabolic fuel for small intestine enterocytes, lymphocytes, macrophages, and fibroblasts. Supplemental use of glutamine, either in oral, enteral, or parenteral form, increases intestinal villous height, stimulates gut mucosal cellular proliferation, and maintains mucosal integrity. It also prevents intestinal hyperpermeability and bacterial translocation, which may be involved in sepsis and the development of multiple organ failure. L-glutamine use has been found to be of great importance in the treatment of trauma and surgery patients, and has been shown to decrease the incidence of infection in these patients. Cancer patients often develop muscle glutamine depletion, due to uptake by tumors and chronic protein catabolism. Glutamine may be helpful in offsetting this depletion; however, it may also stimulate the growth of some tumors. The use of glutamine with cancer chemotherapy and radiotherapy seems to prevent gut and oral toxic side-effects, and may even increase the effectiveness of some chemotherapy drugs.

Digestive System↗
PubMed1997

[Nutritional effects of glutamine-enriched parenteral nutrition on transplanted small intestine in the rat].

We evaluated the preventive effects of glutamine-enriched pareneral nutrition on the atrophy and hypofunction of the transplanted small intestines in the rat. Wistar rats received jejunal isografts and central venous catheters for parenteral nutrition (PN) for ten days. Rats received either PN with 3% alanyl-glutamine or the PN with isonitrogenous ballanced nonessential amino acids. Glutamine-enriched PN significantly increased mucosal villous height mucosal thickness, crypt depth and villous surface area compared with the non-glutamine PN. Normal enterocyte ultrastructure of the graft was maintained in the Glutamine-enriched group. Atrophied microvilli and broken mitochondrial crista were observed in the control group. It was found that the amount of absorption of 15N-glycine was greater at the 1st, 2nd, 3rd hour in glutamine-enriched group than that in the control. These results indicate that the glutamine-enriched parenteral nutrition can promote the proliferation of mucosa, maintain the ultrastructure and improve the amino acid absorption in the transplanted small bowel in the rat.

Animals↗