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R. Fernandes, K. Suzuki, A.K. Kumagai; Inner Blood-Retinal Barrier GLUT1 in Long-Term Diabetic Rats: An Immunogold Electron Microscopic Study . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3907.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: The GLUT1 glucose transporter mediates glucose entry into the endothelial cells of the inner blood-retinal barrier (BRB). In many cell types, exposure to high glucose concentrations or diabetes down-regulates GLUT1. To determine whether long-standing diabetes alters the expression and distribution of inner BRB GLUT1, changes in immunoreactive retinal endothelial cell GLUT1 were studied in Goto-Kakizaki (GK) rats, an animal model of type 2 diabetes. Methods: Immunogold staining for GLUT1 was performed on retinal specimens obtained from 1-year-old GK rats and age-matched Wistar controls. Retinal capillary endothelial cells were visualized by transmission electron microscopy, and GLUT1 immunogold was quantified on the lumenal and ablumenal membranes of endothelial cells from digital microphotographs of individual vessels using a MetaMorph software program. Results: A total of 41 microvessels from 5 diabetic rats and 43 microvessels from 4 non-diabetic Wistar controls were analysed. Densitometric quantification revealed an asymmetry of GLUT1 distribution between lumenal and ablumenal membranes of both diabetic and non-diabetic rats, with a lumen-to-ablumenal ratio of approximately 1 to 3 (p<0.003). The density of retinal endothelial GLUT1 immunoreactivity on the lumenal and ablumenal membranes were not significantly different between the diabetic and control rats. Conclusions: As determined by GLUT1 immunogold electron microscopy, there is no compensatory down-regulation of GLUT1 on the inner-blood retinal barrier in this animal model of long-standing diabetes.
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