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Fig. 7 | Molecular Brain

Fig. 7

From: Metabonomic profiles delineate potential role of glutamate-glutamine cycle in db/db mice with diabetes-associated cognitive decline

Fig. 7

Summary of the metabolic changes in the hippocampus tissue of db/db mice with cognitive decline including glucose metabolism and glutamate–glutamine cycle compared with WT mice. In hyperglycemia circumstance, glycolysis is elevated, while aerobic oxidation is inhibited. As precursor for glutamate, reduction of TCA intermediates, combining with lower levels of glutaminase (GLS) and glutamate decarboxylase (GAD) in neuron, all contributes to the decreased level of glutamate and GABA. The reduced glutamate level, which is consistent with attenuation of postsynaptic glutamate receptors, i.e. N-methyl-D-aspartate (NMDA) subtype, and inhibition of synaptic long-term potentiation (LTP), may contribute to the pathogenesis of diabetes-associated cognitive decline. Keys: glutamate transporter 1 (GLT-1), glutamate aspartate transporter 1 (GLAST-1), sodium-coupled neutral amino acid transporters (SNATs), glucose transporter (Glut 1)

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