Skip to main content
Deletion of GLUT1 in Mouse Lens Epithelium Leads to Cataract Formation
Experimental Eye Research
  • Aditi Swarup
  • Brent A Bell
  • Jianhai Du
  • John Y S Han
  • Jamie Soto
  • E Dale Abel
  • Arturo Bravo Nuevo, Philadelphia College of Osteopathic Medicine
  • Paul G FitzGerald
  • Neal S Peachey
  • Nancy J Philp
Document Type
Publication Date

The primary energy substrate of the lens is glucose and uptake of glucose from the aqueous humor is dependent on glucose transporters. GLUT1, the facilitated glucose transporter encoded by Slc2a1 is expressed in the epithelium of bovine, human and rat lenses. In the current study, we examined the expression of GLUT1 in the mouse lens and determined its role in maintaining lens transparency by studying effects of postnatal deletion of Slc2a1. In situ hybridization and immunofluorescence labeling were used to determine the expression and subcellular distribution of GLUT1 in the lens. Slc2a1 was knocked out of the lens epithelium by crossing transgenic mice expressing Cre recombinase under control of the GFAP promoter with Slc2a1

PubMed ID

This article was published in Experimental Eye Research, Volume 17.

The published version is available at

Copyright © 2018.

Citation Information
Aditi Swarup, Brent A Bell, Jianhai Du, John Y S Han, et al.. "Deletion of GLUT1 in Mouse Lens Epithelium Leads to Cataract Formation" Experimental Eye Research Vol. 17 (2018)
Available at: