Glutamine is the most abundant free amino acid in plasma and tissue pools and an important intermediate in a number of metabolic pathways. Glutamine levels decline markedly in the course of many different catabolic disease states and it has recently been suggested that glutamine may be a conditionally essential dietary nutrient rather than a nonessential amino acid. Changes in tissue glutamine concentrations have been shown to correlate with net protein turnover, and there is evidence that glutamine may both stimulate protein synthesis and inhibit protein degradation. In experimental animals, we have shown that the fall in glutamine concentrations in plasma and tissue pools that occurs in the postoperative state can be prevented or reversed by providing large quantities of exogenous glutamine. In gastrointestinal tissues, the provision of glutamine-free total parenteral nutrition solutions is associated with atrophy of mucosal cells and pancreatic exocrine cells. Glutamine-supplemented parenteral formulas result in diminished atrophy of intestinal mucosal and pancreatic exocrine cells; both intravenous and enteral glutamine promote gastrointestinal tissue regeneration following toxic injury. In animals undergoing partial small intestine resection, glutamine feeding leads to increased adaptive hyperplasia in remaining intestinal segments and results in earlier postoperative weight gain. All of these trophic, anabolic effects of glutamine require the administration of quantities that exceed the glutamine content of normal dietary protein. These findings in experimental animals support the hypothesis that glutamine is a conditionally essential nutrient and suggest a potentially important role for glutamine-supplemented nutrition in catabolic disease states.
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