Glutamine metabolic fate

Figure 4. Schematic representation of the metabolic fate of alanine in hepatocytes. Note that striking differences may exist between mammalian cell types on the one hand and individual amino acids on the other (see text). Solid and broken arrow lines refer to metabolic conversions and transport routes, respectively, and circles in membranes refer to specific transporters. Numbers refer to enzymes involved in alanine metabolism 1, alanine transaminase 2, pyruvate carboxylase 3, malate dehydrogenase 4, glutamate dehydrogenase 5, glutamine synthetase.

Figure 8.17 The metabolism of branched-chain amino acids in muscle and the fate of the nitrogen and oxoacids. The a-NH2 group is transferred to form glutamate which is then aminated to form glutamine. The ammonia required for aminab on arises from glutamate via glutamate dehydrogenase, but originally from the transamination of the branded chain amino acids. Hence, they provide both nitrogen atoms for glutamine formation.

Figure 18.2 Source of glutamine for use by immune celb and cells in the bone and fate of its metabolic products. Glutamine, which is synthesised and stored in muscle, is released and used by the immune cells in lymph nodes and in the wound, and by the cells in the bone marrow. For other tissues that provide glutamine and those that use it, see chapter 8 and see Figure 17.40.

Figure 9-3. Fates of the carbon skeletons upon metabolism of the amino acids. Points of entry at various steps of the tricarboxylic acid (TCA) cycle, glycolysis and gluconeogenesis are shown for the carbons skeletons of the amino acids. Note the multiple fates of the glucogenic amino acids glycine (Gly), serine (Ser), and threonine (Thr) as well as the combined glucogenic and ketogenic amino acids phenylalanine (Phe), tryptophan (Trp), and tyrosine (Tyr). Ala, alanine Cys, cysteine lie, isoleucine Leu, leucine Lys, lysine Asn, asparagine Asp, aspartate Arg, arginine His, histidine Glu, glutamate Gin, glutamine Pro, proline Val, valine Met, methionine.

The ammonia enters the portal vein and mixes with the metabolic nitrogen pool of the body. The fixation of this ammonia nitrogen into arginine, glutamic acid and glutamine and aspartic acid represents a net contribution to nitrogen balance. The alternative fate of this ammonia is its conversion to urea prior to renal excretion. Thus the use of N-labelled ammonium salts or [ N]urea forms the basis of several common lines of clinical investigation. 

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