*** Articoli Scientifici Sulla Glutammina ***
GLUTAMINE
Glutamine is of major importance for muscle metabolism and is a preferred energy source for cells of the intestinal mucosa (Windmueller and Spaeth 1980) and of the immune system, particularly macrophages and lymphocytes (Calder 1994). In catabolic states large amounts of amino acids are released from tissues providing essential substrates for visceral organs for acute phase protein synthesis, urea synthesis and energy production (Gamrin et al. 1996). Despite the accelerated release of amino acids from skeletal muscles, blood glutamine may not be increased after burns (Gore and Jahoor 1994). While intracellular glutamine depletion is typical during malnutrition or varying degrees of stress, there are numerous reports that plasma glutamine concentrations remain normal. Decreased plasma glutamine levels have been reported only after severe burns, multiple trauma or multiple organ failure (Calder 1995, Stinnett et al. 1982). Although increased proteolysis is important for defense against disease, it markedly reduces body stores of proteins and free amino acids (Gamrin et al. 1996), causes serious organ dysfunction and impairs host defense. It has been suggested that depletion of the intracellular pool of free glutamine in burn patients may result from the marked decrease in muscle synthesis of glutamine (Gore and Jahoor 1994). Consequently, glutamine may be "conditionally essential" following burn injury.
A number of studies have shown beneficial effects of supplying glutamine, its precursors (ornithine -ketoglutarate and -ketoglutarate) (Cynober 1991) or glutamine containing dipeptides like alanine-glutamine or glycine-glutamine (Fürst et al. 1990), in quantities corresponding to 25-35% of the dietary protein (Wilmore 1994). Glutamine may improve the clinical response of human patients or lower animals in metabolic stress by increasing nitrogen retention and muscle mass (Stehle et al. 1989), preserving integrity of the intestinal mucosa (Scheppach et al. 1994) and intestinal permeability (van der Hulst et al. 1993), maintaining immunologic function (Calder 1994) and reducing infections (van der Hulst et al. 1996, Ziegler et al. 1992). Some investigators have obtained evidence that glutamine also preserves glutathione levels in liver and other tissues (Fürst 1996b).
Interpretation of the effects of glutamine on bacterial intestinal translocation requires consideration of the types of injury and nutritional support and the method used to detect translocation (Bjarnason et al. 1995; for a review see Lippman 1995). Animal studies have shown that glutamine supplementation decreases bacterial translocation and survival of translocated bacteria and increases animal survival (Gianotti et al. 1995). However, no studies have demonstrated these responses of glutamine supplementation in human patients after burn injury. Lower animals treated with methotrexate, total parenteral nutrition or an elemental diet have shown both positive and negative responses to glutamine supplementation (for a review see Lippman 1995). Although glutamine has been reported to preserve the histological structure of the intestinal mucosa (Scheppach et al. 1994) and intestinal permeability (van der Hulst et al. 1993), its effects on the translocation of intestinal bacteria in patients have not been convincingly shown.
Parry-Billings et al. (1990) reported that plasma glutamine levels of burn patients decreased by 58% and remained depressed for 21 d after injury. Their culture experiments showed that the depressed glutamine concentrations were associated with significantly reduced proliferation of lymphocytes from healthy volunteers and phagocytosis by peritoneal macrophages from normal mice. They suggested that the reduction of plasma glutamine may reduce immunologic competence after burn injury. Ogle et al. (1994) also reported that glutamine improved the bactericidal ability of abnormal neutrophils from pediatric patients after burns.
Although Parry-Billings et al. (1990) and Ogle et al. (1994) suggested the efficacy of glutamine supplementation, they did not supply it to their patients. We have also not found evidence of its use after burn injury. However, when 10-30 g/d ornithine -ketoglutarate were administered, nitrogen balance improved, plasma phenylalanine and urinary 3 methyl-histidine decreased, serum proteins rose and clinical outcomes improved (Cynober 1991). Because ornithine -ketoglutarate increases muscle, hepatic and plasma glutamine in burn victims (Le Bricon et al. 1997), some of the positive response may be the result of glutamine repletion. These effects of glutamine and the severe depletion of intracellular glutamine after injury, deserve further investigation.
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