The effect of enterectomy on postoperative visceral organ glutamine exchange was studied in order to gain further understanding of the role of the intestinal tract in the altered glutamine metabolism that occurs following catabolic illness. In addition to studying glutamine, which transports 1 3 of whole blood amino acid nitrogen, we determined the fluxes of glutamate and alanine across the gastrointestinal tract, liver, and kidneys in 18 postoperative dogs. Arterial glutamine and glutamate were significantly higher in enterectomized animals than in controls. With enterectomy the gut became an organ of glutamine balance while in control dogs the GI tract consumed glutamine (0.11 ± 0.04 vs 1.67 ± 0.14 μmole/kg · min, P < 0.001). The gut switched from an organ of glutamate release to one of net glutamate uptake following enterectomy and intestinal alanine release simultaneously fell by 50%. Simultaneously, the liver reduced its uptake of alanine and became an organ of glutamine release. Renal glutamine consumption was also diminished in enterectomy animals. The interorgan exchange of glutamine and other amino acids is altered by enterectomy. The increase in circulating glutamine levels in enterectomized animals suggests that the accelerated intestinal glutamine consumption that characterizes catabolic illnesses contributes to the low glutamine levels in these stress states. In addition, it becomes apparent that the gut is an important supplier of alanine to the liver, which supports gluconeogenesis. Metabolic adaptation and cooperation between organs is essential during organ absence or dysfunction if the organism is to survive critical illness.
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