Glutamine plasma level

One trick is the administration of benzoate or phenylac-etate. These acids react with glycine or glutamine, respectively, to produce complexes (conjugates) which are excreted in the urine (Figure 10.10). This decreases the plasma level of either of these non-essential amino acids... 

To date, several small molecule biomarkers of renal toxicity have been described in the literature. Urine composition is considered to reflect kidney function and pathology. Thus, in the presence of proximal tubule damage, the relative concentrations of a number of metabolites (glucose, lactate, alanine, lysine, glutamine, glutamate, and valine) are markedly increased due to impaired reabsorption of those metabolites. An increase in the relative concentrations of those metabolites in urine is typically accompanied by a corresponding decrease in plasma levels [50,55],... 

Figure 17.39 Effect of changes in glutamine levels in culture media on proliferation of human lymphocytes. The numbers represent the concentration of glutamine, in (xmol/L, in culture media. Note that both the maximum rate and the rate of response are decreased as the glutamine concentration in culture medium is decreased. The plasma glutamine level in normal humans is 600 (xmol/L.

Table 18.5 Plasma glutamine levels in normal subjects and patients...

The anorexia suffered by cancer patients is likely to arise from a combination of psychological stress, altered senses of taste and smell and increased levels of cytokines, which influence the appetite and satiety centres in the hypothalamus. There are several consequences micronutrient intake will be diminished and this may contribute to the signs and symptoms of the disease. Plasma amino acid levels will fall, as in starvation (Chapter 16). Synthesis of glutamine (by muscle, adipose and lung), aspartate (by liver), glutathione (by the intestine) and arginine (by the kidney) will all be compromised. The metabolic significance of all of these is discussed in Chapter 18. 

CSF amino acids do not show an important age dependence (Table 2.1.7). Levels of most amino acids in the CSF are much lower than in the plasma, the exception being glutamine. The low CSF values bear a certain analytical risk a traumatic lumbar puncture will result in the presence of small amounts of blood in the CSF. This readily influences the CSF amino acid levels and should be interpreted with care. In contrast with some of the neurotransmitter metabolites, no ventral/dorsal gradient for the amino acid is observed. 

All enteral feeds were stopped. The baby was given intravenous glucose, L-arginine, sodium benzoate, and sodium phenylacetate. Hemodialysis was initiated. At this time, there were no spontaneous respirations, there was no response to painful stimuli, and brainstem reflexes were absent. The plasma amino acid results revealed a glutamine level of 1500 pmol/L (normal 254-823), and citrulline was undetectable (normal 10-34 pmol/L). Quantitative carnitine, plasma acylcarnitine, and urine organic acid profiles were normal. The urine orotic acid concen-... 

The blood alanine level is also always increased, sometimes markedly to about 2-4 times the normal value (L3, L6). This is presumably because the normal transamination of alanine to pyruvate, which requires a-ketoglutarate, is inhibited both by the excess of glutamine in the blood and by the drain on a-ketoglutarate. One other amino acid, camosine, has been found to be present in the plasma or in raised amounts in the urine, in those cases of hyperammonemia where it has been sought (LIO). There are no consistent changes in any of the other amino acids, including lysine, in the blood. 

The changes in levels of amino acids other than glutamine in the cerebrospinal fluid in hyperammonemia are variable. In two reported instances (L3, L6), the arginine level was low, 30-50% of the normal. This could be a reflection of the decreased plasma arginine level or possibly of the block in the urea cycle in the brain itself. On the other hand, in another instance (LIO), the arginine level was normal. The changes in the other amino acids are also not consistent. In any case, the cerebrospinal fluid levels of amino acids are so low that such changes as were found are difiicult to interpret with certainty (Table 6). 

In the first case of citrullinemia reported (M6), intermediary metabolites of the pyrimidine pathway were not sought in the urine. In the second, orotic acid was tested for, but not detected (M12). In the third child, orotic acid, uridine, and uracil were found in relatively large amounts in the urine when the plasma glutamine was at the very high level of 41.0 mg/100 ml, showing that in this genetic disorder, as in the other disorders of urea synthesis, these metabolites are always excreted in excess when the glutamine is raised (VI). 

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