Glutamine in the liver and kidney is catabolized to glutamate and ammonia with the help of the enzyme glutaminase.1,2 In the absorptive state or during periods of alkalosis, liver glutaminase activity increases ammonia production for the urea cycle.1,2 Under the acidotic state, use of glutamine in the urea cycle decreases, and instead, glutamine is released from the liver and transported to the kidneys, where it is catabolized by the renal tubular enzyme glutaminase to produce ammonium and glutamate.12 This glutamate may be catabolized by the enzyme glutamate dehydrogenase to produce a-ketoglutarate, which can be used for energy production via the citric acid cycle or nonessential amino acid synthesis via the transamination process, and ammonium.12
Iwashita et al.34 observed that glutamine supplementation to exercising dogs stimulated whole-body glucose production during and after exercise above a normal exercise response by 24%. Hepatic uptake of glutamine and alanine was higher with glutamine supplementation during exercise, and hepatic glucose output was increased sevenfold during exercise with glutamine supplementation. Glutamine supplementation was observed to increase glucose utilization by 16% after exercise, suggesting that glutamine availability can modulate glucose homeostatis during and after exercise. Renal glutaminase activity and ammonium excretion increase with acidosis and decrease with alkalosis.12 Thus, given the ubiquitous synthesis of glutamine in the cells and its ability to diffuse in and out of cells, it serves as a major transporter of nitrogen.
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