Here we report multiple lines of evidence for a comprehensive model of energy metabolism in the vertebrate eye. Metabolic flux, locations of key enzymes, and our finding that glucose enters mouse and zebrafish retinas mostly through photoreceptors support a conceptually new model for retinal metabolism. In this model, glucose from the choroidal blood passes through the retinal pigment epithelium to the retina where photoreceptors convert it to lactate. Photoreceptors then export the lactate as fuel for the retinal pigment epithelium and for neighboring Müller glial cells. We used human retinal epithelial cells to show that lactate can suppress consumption of glucose by the retinal pigment epithelium. Suppression of glucose consumption in the retinal pigment epithelium can increase the amount of glucose that reaches the retina. This framework for understanding metabolic relationships in the vertebrate retina provides new insights into the underlying causes of retinal disease and age-related vision loss.
- James B Hurley
- James B Hurley
- Jianhai Du
- Jennifer R Chao
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Animal experimentation: All animal research was authorized by the University of Washington Institutional Animal Care and Use Committee.
- Ralph DeBerardinis, Reviewing Editor, UT Southwestern Medical Center, United States
- Received: May 22, 2017
- Accepted: September 12, 2017
- Accepted Manuscript published: September 13, 2017 (version 1)
© 2017, Kanow et al.
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