Regulation of GLUT-3 glucose transporter in the hippocampus of diabetic rats subjected to stress

Previous studies from our laboratory have demonstrated that chronic stress produces molecular, morphological, and ultrastructural changes in the rat h ippocampus that are accompanied by cognitive deficits. Glucocorticoid atten uation of glucose utilization is proposed to be one of the causative factor s involved in stress-induced changes in the hippocampus, producing an energ y-compromised environment that may make hippocampal neuronal populations mo re vulnerable to neurotoxic insults. Similarly, diabetes potentiates neuron al damage in acute neurotoxic events, such as ischemia and stroke. Accordin gly, the current study examined the regulation of the neuron-specific gluco se transporter, GLUT-3, in the hippocampus of streptozotocin-induced diabet ic rats subjected to restraint stress. Diabetes leads to significant increa ses in GLUT-S mRNA and protein expression in the hippocampus, increases tha t are not affected by stress. Collectively, these results suggest that stre ptozotocin-induced increases in GLUT-3 mRNA and protein expression in the h ippocampus may represent a compensatory mechanism to increase glucose utili zation during diabetes and also suggest that modulation of GLUT-S expressio n is not responsible for glucocorticoid impairment of glucose utilization.