Retina accumulates more glucose than does the embryologically similar cerebral cortex in diabetic rats

Aims/hypothesis. The retina is embryologically similar to cerebral cortex a nd the tissues of both are exposed to similar blood glucose concentrations. Nevertheless, in diabetes the retina develops metabolic abnormalities and microvascular lesions from which cerebrum seems relatively protected. We di rectly compared glucose concentrations and expression of GLUT-I (the major carrier transporting glucose from blood into the neural retina and cerebrum ) in the two tissues from normal and diabetic rats. Methods. Tissue and intracellular glucose were measured using two methods: direct assay of glucose and assay of Amadori products on intracellular prot eins. The expression of GLUT-1 was measured using western blots in tissue a nd in the isolated endothelial luminal membrane of the two vascular beds. Results. Both methods assessing intracellular glucose indicate that intrace llular concentrations of glucose in diabetes increased significantly in the retina but not in cerebral cortex. Concentrations of free glucose and Amad ori product in retinas of diabetic animals were increased above normal by 3 34 % and 122 %, respectively, whereas there was no statistically significan t increase in either parameter in the cerebral cortex of diabetic animals. In contrast to the observed increase in glucose in the retina in diabetes, expression of GLUT-1 on the luminal plasmalemma of the retinal vascular end othelium and in homogenates of whole retina decreased to a statistically si gnificant extent (55 % and 36 %, respectively compared to normal). In the l uminal cell membrane of the cerebral vasculature, diabetes did not decrease expression of GLUT-1 but tended to increase it slightly. Conclusions/interpretation. Even among tissues that do not require insulin for glucose uptake, tissue glucose concentration varies in diabetes. The gr eater increase in glucose concentration in retina than in cerebrum in diabe tes probably contributes to the tissue differences in biochemical and histo pathologic sequelae of the disease. The expression of GLUT-1 in the microva sculature is unlikely to account for the differences in tissue glucose betw een retina and cerebrum.