Glutamine is the most abundant amino acid in the blood and is an important source of energy for many tissues in the body. It is derived from the amino acids histidine and glutamic acid.
– Glutamine acts as a precursor to glutamate and GABA.
– Glutamine is derived directly from dietary protein, and also formed endogenously by addition of ammonia to glutamate.
– Glutamine aids in the maintenance of: gut barrier function, intestinal cell proliferation, and differentiation.
– Optimal glutamine levels are important for intestinal function.
– In the central nervous system the formation of glutamine from glutamate provides a disposal mechanism that protects against excess accumulation of cytotoxic ammonia.
References:
Low glutamine can be a result of:
– protein malnutrition
– negative nitrogen balance
– incomplete digestive proteolysis
– other malabsorption syndromes
– chronic alcoholism.
Glutamine can also be low as a result of sample decay in which glutamine is broken down to glutamate and ammonia due to improper, post-collection preservation and handling of the blood specimen.
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– High levels may be a sign of inhibitory/excitatory imbalances in the neurotransmitter system.
– High glutamine levels are thought to be a signal for imbalances within the nervous system.
– High glutamate can be marker of vitamin B6 deficiency.
– Ammonia accumulation suspected if low or low normal glutamic acid. Extra á-KG needed to combine with ammonia and to make up for energy deficit caused by over-utilization of á-KG to deal with toxic ammonia levels.
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High protein intake may contribute to higher levels. It should also be noted that glutamine is available as a nutraceutical supplement. Elevations can also be seen with supplementation. The metabolism of glutamine requires several cofactors, such as NADPH and vitamin B1.
Functional deficiencies of vitamin and mineral cofactors can also elevate levels. There is literature to suggest vitamin B1 supplementation lowers elevated levels of glutamine, as well as other amino acids in thiamine deficiency. Because of the relationship of glutamine and glutamate to both the Cahill Cycle and Urea Cycle, elevations of glutamine are associated with hyperammonemia due to increased production of glutamine from glutamate.
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1-Methylhistidine (Plasma), 3-Methylhistidine (Plasma), Alanine (Plasma), Alpha-Amino-n-butyric acid (Plasma), Alpha-Aminoadipic Acid (Plasma), Alpha-ANB/Leucine, Anserine (Plasma), Arginine (Plasma), Asparagine (Plasma), Aspartic Acid (Plasma), Beta-Alanine, Beta-Aminoisobutyric Acid (Plasma), Carnosine (Plasma), Citrulline, Cystathionine (Plasma), Cystine, Ethanolamine (Plasma), g-Aminobutyric Acid (Plasma), Glutamic Acid (Plasma), Glutamic Acid/Glutamine, Glutamine (Plasma), Glycine (Plasma), Histidine (Plasma), Homocysteine (Genova), Homocystine (Genova), Hydroxylysine (Genova), Hydroxyproline (Genova), Hydroxyproline/Proline (Genova), Isoleucine (Plasma), Leucine (Plasma), Lysine (Plasma), Methionine (Plasma), Ornithine (Genova), Phenylalanine (Plasma), Phenylalanine/Tyrosine (Genova), Phosphoethanolamine (Plasma), Phosphoserine (Plasma), Proline (Plasma), Sarcosine (Plasma), Serine (Plasma), Taurine (Plasma), Threonine (Plasma), Tryptophan (Plasma), Tryptophan/LNAA (Genova), Tyrosine (Plasma), Valine (Plasma)
