hepatocytes, where it plays a major role in whole body glutamine production. The enzyme glutaminase is abundant in enterocytes (particularly in jejunum), in brain, kidney, and other tissues. In the cytoplasm of periportal hepatocytes, glutaminase is activated in response to increased portal vein concentrations of glutamine derived from the intestinal lumen (11).
increases renal uptake significantly (33). Approximately 60% to 85% of the glutamine that is absorbed from the GI lumen of healthy humans is captured and presumably metabolized by the splanchnic bed (34, 35). Plasma glutamine concentrations rise in a dose-dependent fashion after oral glutamine loads (34, 35). In addition, enterally administered glutamine is metabolized by splanchnic tissues to amino acid end products. In one study, healthy adults given a single oral bolus dose of L-glutamine (0, 0.1, and 0.3 g/kg) showed a dose-related increase in plasma levels of alanine, citrulline, and arginine (converted from citrulline in kidney) (34). Tracer studies in healthy adults showed intestinal consumption of glutamine at a rate that depended on glutamine supply (36). Approximately 13% of glutamine taken up by the intestines was converted to citrulline, and glutamine was the only important precursor for intestinal citrulline release (36). In stable isotope studies, whole body glutamine use was reduced approximately 20% in patients with extensive small intestinal resection (37).
TABLE 34.1 MAJOR METABOLIC FUNCTIONS OF GLUTAMINE
requirements of some patients during catabolic illness because glutamine is absent in standard PN and present in low quantities in most EN formulations (1, 7, 9). Elegant interorgan studies by Souba et al (10, 11, 16) showed that following operative trauma, the efflux of glutamine from the lung and, especially, from muscle was accelerated to provide glutamine to wounds, the gut, immune cells, kidneys (for renal ammoniagenesis), and liver. These effects were mediated by the rise that occurs in glucocorticosteroids in blood. In sepsis, a more dramatic release of glutamine from muscle and, to a lesser extent, from lung was noted. Immune system cells and liver appeared to be the major consumers of glutamine, whereas glutamine uptake in the gut and kidney was diminished (10, 11, 16). Studies in humans confirmed that high doses of glucocorticoids increase glutamine extraction by the splanchnic bed, presumably secondary to a regional increase in glutamine requirements (16, 17).