May 1994
Volume 35, Issue 6
Articles  |   May 1994
GLUT1 glucose transporter expression in the diabetic and nondiabetic human eye.
Author Affiliations
  • A K Kumagai
    Department of Medicine, UCLA School of Medicine 90024.
  • B J Glasgow
    Department of Medicine, UCLA School of Medicine 90024.
  • W M Pardridge
    Department of Medicine, UCLA School of Medicine 90024.
Investigative Ophthalmology & Visual Science May 1994, Vol.35, 2887-2894. doi:
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      A K Kumagai, B J Glasgow, W M Pardridge; GLUT1 glucose transporter expression in the diabetic and nondiabetic human eye.. Invest. Ophthalmol. Vis. Sci. 1994;35(6):2887-2894.

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PURPOSE: The GLUT1 glucose transporter is expressed in endothelial and epithelial barriers, including the retinal capillary endothelium and the retinal pigment epithelium (RPE) of the eye. The present studies were undertaken to determine whether GLUT1 is expressed in additional cell types within the human eye and whether retinal endothelial GLUT1 is aberrantly expressed in diabetic proliferative retinopathy in humans. METHODS: Immunohistochemical staining of sections of human eyes obtained at surgery or autopsy from patients with and without diabetes was performed with polyclonal antisera directed against the human GLUT1 glucose transporter. RESULTS: In the course of this study, an unexpected multicellular localization of GLUT1 in different cellular barriers of the human eye was observed. In the nondiabetic eye, specific staining for GLUT1 was seen in the nerve fiber layer, the ganglion and photoreceptor cell bodies, the capillaries and the RPE of the retina, the basal infoldings of the pigmented and nonpigmented layers of the ciliary body, the capillary endothelium and posterior epithelium of the iris, the corneal epithelium and endothelium, and the endothelium lining of the canal of Schlemm. Müller cells, a type of retinal glial cell identified by morphology and by parallel staining for glial fibrillary acidic protein, also stained intensely positive for GLUT1. The pattern of GLUT1 immunoreactivity in the diabetic eyes was virtually identical to that in the nondiabetic specimens, with the notable exception that the neovascular endothelium of proliferative retinopathy did not stain for GLUT1. CONCLUSIONS: These studies describe the heretofore unrecognized expression of immunoreactive GLUT1 in the ganglion cell layer of the retina, the endothelium lining the canal of Schlemm, the corneal endothelium, and the basal cells of the corneal epithelium of the human eye. The present study also provides evidence for immunoreactive GLUT1 in glial cells of the central nervous system. Because the expression of GLUT1 is characteristic of tissues that possess a barrier function, the absence of GLUT1 immunoreactivity in the neovascular tissue of proliferative diabetic retinopathy suggests that the loss of selective permeability is associated with an absence of facilitated glucose transport in this disorder.


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