Document Type

Article

Publication Date

1-16-2026

Comments

This article is the author’s final published version in iScience, Volume 29, Issue 1, 2026, Article number 114450.

The published version is available at https://doi.org/10.1016/j.isci.2025.114450. Copyright © 2025 The Authors.

Abstract

GLUT1 facilitates a continuous flow of glucose across the inner and outer blood-retinal barriers (BRBs) to support vision. To understand the extent to which photoreceptors rely on glucose transport across the outer BRB, we generated a tamoxifen-inducible conditional knockout of Slc2a1 in the retinal pigment epithelium (RPE) (RPE-iΔGlut1). In the RPE-iΔGlut1 mice, rod photoreceptors exhibited impaired outer segment renewal and decreased the expression of proteins involved in phototransduction and ciliary transport. Proteins regulating the retinal stress response increased. Cone photoreceptors were functional and viable 15 months post-tamoxifen treatment in the RPE-iΔGlut1 mice, while 70% of the rods died. When Slc2a1 was genetically deleted from rods (Rod-iΔGlut1 mice), rod degeneration was faster than in the RPE-iΔGlut1 mice. These findings suggest that rods are more dependent on glucose than cones, and that glucose from the deep vascular plexus may support cone function and viability and slow the rate of rod death.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

PubMed ID

41550716

Language

English

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