Biochemical adaptations of the retina and retinal pigment epithelium support a metabolic ecosystem in the vertebrate eye

Elife. 2017 Sep 13;6:e28899. doi: 10.7554/eLife.28899.

Abstract

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.

Keywords: biochemistry; energy metabolism; mouse; neuroscience; photoreceptors; retina; zebrafish.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adaptation, Ocular*
  • Animals
  • Energy Metabolism*
  • Ependymoglial Cells / metabolism
  • Ependymoglial Cells / physiology*
  • Glucose / metabolism
  • Humans
  • Lactates / metabolism
  • Mice
  • Photoreceptor Cells / metabolism
  • Photoreceptor Cells / physiology*
  • Retinal Pigment Epithelium / metabolism
  • Retinal Pigment Epithelium / physiology*
  • Zebrafish

Substances

  • Lactates
  • Glucose