Have We Enough Glutamine and How Does It Work? A Clinician’s View

Abstract

There is a gap between the scientific basis of the claim that in several disease states glutamine is lacking and the widespread belief that supplementation of glutamine to the nutritional regimen is beneficial in severely ill patients. Glutamine shortage exists when consuming tissues, playing a crucial role in the response to trauma and disease, receive insufficient amounts of glutamine. In these tissues (immune system, wound), glutamine is only partly oxidized but has more specific roles as nontoxic nitrogen carrier, precursor of several crucial metabolites required for cell proliferation and for maintenance of the redox potential, and as osmolyte. In inflammatory states, glutamine concentrations in plasma and tissues are decreased due to many disease-related factors, precluding its use as a reliable indicator of shortage. Isotope studies have yielded equivocal results, precluding their use as a reliable indicator of glutamine shortage or adequacy. The increase in the net release of glutamine from peripheral tissues to central tissues (immune system, liver, spleen, wound) in inflammatory states provides a better basis for the necessity to supplement the organism with extra glutamine in these conditions. Glutamine supplementation was beneficial in a few studies in burn or trauma patients. The clinical benefit of parenteral glutamine supplementation in patients with severe inflammation has been demonstrated more convincingly. The amounts of glutamine supplemented approximate the amounts released by peripheral tissues and utilized by central organs operative in host defense and are therefore in the physiological range.

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

“…In colonic cancer patients undergoing surgery, plasma glutamine levels drop by 30 %, independently of the previous glutamine depletion [296]. In severe pancreatitis [297] and trauma patients [298], plasma glutamine levels decrease to less than 50 % of its basal levels as compared to control values. Similar effects have also been seen in experimental animal models of sepsis, followed by severe adaptive immune system suppression (low T and B lymphocyte responses) [50,209,299].…”

Nutrition and Chronic Wounds: Improving Clinical Outcomes

“…In these cells of rapid turnover, nitrogen may be used in the production of needed amino acids, and purines and pyrimidines for DNA and RNA synthesis. 81 Its metabolic functions include provision of NADPH and increasing insulin sensitivity. 81 Glutamine also appears to have a role in leukocyte apoptosis, superoxide production, antigen processing, and phagocytosis.…”

“…81 Its metabolic functions include provision of NADPH and increasing insulin sensitivity. 81 Glutamine also appears to have a role in leukocyte apoptosis, superoxide production, antigen processing, and phagocytosis. 82,83 The suggested anti-inflammatory and immune activity may include activation of Figure 8.…”

“…In these cells of rapid turnover, nitrogen may be used in the production of needed amino acids, and purines and pyrimidines for DNA and RNA synthesis. 81 Its metabolic functions include provision of NADPH and increasing insulin sensitivity.…”

Reduced Glutamatergic Neurotransmission as Possible Indicator of Unfavorable Prognosis

“…Factors of the "generalized" hypoaminoacidemia in the development of a patient's critical condition are the increased AA distribution due to vasodilation and increased permeability of the endothelium, an inhibition of the synthesis of a number of AAs in the liver and their increased consumption in central tissues (immune system, liver, spleen, wound). [46,87] Experimental data have shown that stress factors increased the KYNA formation and other metabolites of KP of tryptophan catabolism by activating the secretion of glucocorticoids and a significant increase in the activity of TDO [88] and IDO, which is regulated by cytokines. [89] The increased KYNA concentration after acute physiological stress was observed in clinical studies performed by E. KotlinskaHasiec et al…”