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L. Zheng, W. Zheng, P. Rao, Y.–Z. Le; Glucose Transport in the Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3047.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Retina is the most active tissue metabolically and is entirely dependent on glucose to generate ATP under normal conditions. To study the function of glucose transporters in glucose utilization and metabolism and diabetic retinopathy, we decided to 1) investigate the expression of glucose transporters in ARPE–19 cell lines and 2) establish mouse models of the major blood barrier glucose transporter (GLUT1) null in a number of retinal cell–types using a variety of retinal cell–type specific Cre mice established in our laboratory. Methods: RT–PCR analysis of differentiated ARPE–19 cell line was used to determine the expression of glucose transporters. A clone of bacterial artificial chromosome (BAC) carrying the mouse GLUT1 genomic DNA was identified with sequence analysis and confirmed with PCR and Southern blot analysis. The mouse GLUT1 gene was cloned from the BAC with conventional cloning methods. Results: RT–PCR analysis suggested the presence of multiple glucose transporters in the ARPE–19 cells. A 12–kb mouse genomic DNA covering GLUT1 exon 2–10 was cloned from BAC to generate temporal and spatial GLUT1 null mice. A ten–step–construction of Cre/lox conditional gene targeting vector is in progress. Conclusions: The presence of multiple glucose transporters in the ARPE–19 cells suggests a potential compensatory mechanism for glucose transport through the RPE to the retina. Generation of Cre/lox conditional GLUT1 knockout mice will allow us to examine the presence of compensatory glucose transport mechanisms and dissect GLUT1 function in vivo.
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