Brain glutamine synthesis requires neuronal aspartate: a commentary.
Inspired by the paper, 'Brain glutamine synthesis requires neuronal-born aspartate as amino donor for glial glutamate formation' by Pardo et al, a modified model of oxidation-reduction, transamination, and mitochondrial carrier reactions involved in aspartate-dependent astrocytic glutamine synthesis and oxidation is proposed. The alternative model retains the need for cytosolic aspartate for transamination of α-ketoglutarate, but the 'missing' aspartate molecule is generated within astrocytes during subsequent glutamate oxidation. Oxaloacetate formed during glutamate formation is used during glutamate degradation, and all transmitochondrial reactions, oxidations-reductions, and cytosolic and mitochondrial transaminations are stoichiometrically balanced. The model is consistent with experimental observations made by Pardo et al.
Department of Clinical Pharmacology, College of Basic Medical Sciences, China Medical University, Shenyang, PR China. leifhertz@xplornet.ca
Leif
L
Hertz
D001224:Aspartic Acid / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism; D001923:Brain Chemistry / Q000502:physiology*; D005973:Glutamine / Q000096:biosynthesis*; D006801:Humans; D007656:Ketoglutaric Acids / Q000378:metabolism; D008293:Malates / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010084:Oxidation-Reduction
D007656:Ketoglutaric Acids; D008293:Malates; D005973:Glutamine; D001224:Aspartic Acid; C030298:malic acid