Alpha-aminoadipic acid (a-Aminoadipic acid) is an intermediary metabolite of lysine (primarily) and tryptophan.
Alpha-aminoadipic acid also is a metabolite of yeast/fungi metabolism, and anecdotal evidence supports occasional increases with intestinal dysbiosis as a source.
In Reye’s syndrome, alpha-aminoadipic hyperaminoaciduria occurs together with hyperlysinuria. Rare metabolic and acute alpha-aminoadipic hyperaminoaciduria is documented as a hereditary defect in the Alpha-aminoadipic acid transaminase enzyme and the next enzyme in the sequence, alpha-ketoadipic acid dehydrogenase.
In glutaric acidemia/aciduria, there can be notable alpha-aminoadipic hyper-aminoaciduria due to a hereditary weakness of glutaryl CoA dehydrogenase. Riboflavin insufficiency as FAD may provoke or worsen alpha-aminoadipic hyperaminoaciduria (and glutaric acidosis) if the dehydrogenase enzymes are weak. Still, riboflavin may or may not improve the kinetics of defective dehydrogenases.
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