Here is a run down ont the benefits of glutamine as for an anabolic effect though it
helps those with illness and serious aa loss for a health athlete benefits are extremely doubtful
. MECHANISM OF ACTION
1. SUMMARY: Glutamine has traditionally been considered a non-
essential amino acid. It is the most abundant amino acid in the body. Glutamine stimulates anabolism of protein and inhibits catabolism of protein. Glutamine is essential for maintaining intestinal function, the immune response, and amino acid homeostasis. Glutamine serves as a metabolic fuel for rapidly proliferating cell lines such as enterocytes, colonocytes, fibroblasts, lymphocytes, and macrophages (Fraga Fuentes et al, 1996). Glutamine inhibits net protein loss and protein breakdown in muscle (MacLennan et al, 1988). The body is depleted of glutamine stores during trauma, hypercatabolism, immunodeficiency, malnutrition or extreme stress and in these states it may be considered an essential amino acid (Lacey, 1990). Glutamine has been shown to support immune function, to protect oral and gastrointestinal mucosa from iatrogenic injury during radiation and chemotherapy, and to decrease tumor activity in an animal model (Jones et al, 1999; Houdijk et al, 1998; Anderson et al, 1998; Klimberg et al, 1996). It has also been found to protect lymphocyte counts and reduce gut permeability in advanced esophageal cancer patients receiving radiochemotherapy (Yoshida et al, 1998). Glutamine also caused an increase in T-cell DNA synthesis in postoperative surgical patients receiving total parenteral nutrition (O'Riordain et al, 1994).
2. ANABOLIC EFFECT:
a. Glutamine is produced in
skeletal muscle from glutamate and ammonia catalysed by glutamine synthetase. Glutamate can be obtained from circulation, breakdown of protein, or a catalyzation process (Rohde et al, 1996).
b. Skeletal muscle contains up to 60% of total body glutamine stores. Glutamine is released into circulation during metabolic stress, trauma, and surgery. Glutamine muscle concentration is affected by injury, sepsis, prolonged stress, and starvation (Miller, 1999). Plasma glutamine levels decrease after severe organic injuries partly because the small intestine uses it faster than it can be produced by skeletal muscle (Cukier et al, 1999).
c. Hormones, concentrations of electrolytes, and branched-chain amino acids influence a transport mechanism allowing glutamine to be released by crossing the cell membrane. Glutamine intracellular concentration changes are an early sign of skeletal muscle protein catabolism (Vinnars et al, 1990; MacLennan et al, 1988).
3. ANTIBACTERIAL EFFECT:
a. Glutamine treated trauma patients had increased plasma glutamine concentrations as well as increased concentrations of both citrulline and arginine suggesting that glutamine caused stimulation of renal production of arginine. In rats, glutamine has been shown to stimulate the renal production of arginine by raising plasma concentrations of the precursor citrulline. Arginine has been shown to stimulate lymphocyte immune responses and wound healing. Soluble tumor necrosis factors p55 and p75 were also lower compared to controls suggesting a lower systemic inflammatory response. All of these were found parallel with a decreased number of infectious complications (Houdijk et al, 1998).
4. ANTIOXIDANT EFFECT:
a. Glutamine is manufactured in the liver from glutamate, cysteine, and glycine. It is an extremely important substrate in supporting liver detoxification processes and acts as a powerful antioxidant protecting hepatocytes. Acute poisoning and high dose chemotherapy in bone marrow transplantation can cause patients to suffer from hepatic failure. Glutamine supplementation has been shown to preserve glutathione liver stores and protect the liver from free radical damage after acute toxicity from acetaminophen poisoning and high-dose cytotoxic therapy during bone marrow transplants (Hong et al, 1992; Brown et al, 1998).
5. DIGESTIVE SUPPORT:
a. Glutamine has been found to diminish electrolyte and water loss during acute bouts of diarrhea. An animal in vitro study suggested that this effect was likely due to increased stimulation of sodium and sodium chloride transport in piglet rotavirus-damaged jejunum. Glutamine functioned as a dual transporter crossing the cell membrane attached to sodium (electrogenic effect). It also stimulated electroneutral absorption of sodium chloride (Rhoads et al, 1991). In a study of patients with human immunodeficiency virus, L-glutamine 4 and 8 grams per day reduced intestinal permeability, diarrhea, and secondary infections but did not improve intestinal morphology and inflammation (Noyer et al, 1998).
6. IMMUNE SYSTEM ENHANCEMENT:
a. Lymphocyte reactivity was higher after mice received a diet enriched in glutamine. Mice were fed a glycine-enriched diet (glutamine 13.3 grams/kilogram) for 2 weeks. Increasing the amount of glutamine in the diet increased the ability of T-lymphocytes to respond to mitogenic stimulation. Increasing the oral availability of glutamine may promote the T-cell immune response (Kew et al, 1999).
b. An in vitro study found that glutamine increased the production of interleukin-2 and gamma interferon which is important for optimal lymphocyte proliferation (Rhohde et al, 1996). Glutamine supplementation caused an increase in T-cell synthesis in postoperative surgical patients receiving total parenteral nutrition (O'Riordain et al, 1994). Prolonged parenteral nutrition has been found to cause a significant decrease in secretory Immunoglobulin A (IgA), gut lamina plasma IgA, CD4 and CD8 lymphocytes in the intestinal tract. Glutamine-supplemented parenteral nutrition prevented the reduction of both B- and T-cell lines when compared to glutamine deficient parenteral nutrition in an animal study (Alverdy et al, 1992).
7. TUMOR INHIBITION/CHEMOPROTECTIVE EFFECT:
a. L-glutamine supplementation increased glutathione (GSH) levels, decreased pro-inflammatory prostaglandin E2 (PGE2) production, increased natural killer (NK) activity by 2.5 times and resulted in a 40% decrease in tumor growth in a rat breast cancer model (Klimberg et al, 1996). Serum levels of L-glutamine in gastric carcinoma patients were reduced when compared to controls in a Russian study (Anderson et al, 1998). Glutamine supplementation increased the cytoxicity of methotrexate. An animal study showed a 300% increase in the therapeutic delivery of methotrexate to targeted tumor cells. Glutamine increased the therapeutic window of methotrexate and 5-FU while protecting the patient from the gastrointestinal adverse effects of the drug (Rubio et al, 1998).
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