# Control of Photoreceptor Metabolism

> **NIH NIH R01** · UNIVERSITY OF WASHINGTON · 2024 · $441,250

## Abstract

Project Summary/Abstract
Photoreceptors consume glucose rapidly because they derive about half of their
metabolic energy from the inefficient process of aerobic glycolysis. The retinal pigment
epithelium (RPE) is the blood barrier for the outer retina, so glucose from the circulation
must pass through it to reach the retina. The ability of the RPE to transport and recycle
fuel is essential for homeostasis of the outer retina. Deficiencies in its functions caused
either by genetics, by environment factors or by aging cause vision loss.
Whereas photoreceptors extract energy from glucose by aerobic glycolysis, the
metabolic features of the RPE are complementary. The RPE uses its mitochondria to
minimize its own consumption of glucose, presumably so that more glucose can pass
through it to reach the retina.
Research on retina and RPE metabolism has focused mostly on the immediate use of
fuels. However, cells also store metabolic energy, either as glycogen or as fat. RPE cells
have both, but we do not know yet how depots of glycogen and fat contribute to normal
retina and RPE metabolism and homeostasis.
The metabolic relationships between the retina and RPE vary throughout day. We will
use both ex vivo and in vivo strategies to quantify diurnal changes in metabolic flux and
energy storage in RPE/choroid tissue. In the first aim we will identify diurnal influences
on glycogen metabolism. In the second aim we will identify diurnal influences on fatty
acid metabolism and in the third aim we will evaluate effects on stored fuels of mutations
that cause photoreceptor degeneration and that disrupt RPE phagocytosis.
Understanding how the metabolic state and the source of energy, either from blood or
from fuels stored in the RPE, may vary with a diurnal or circadian cycle may in future
studies be used to develop metabolism-based strategies that make photoreceptors more
resilient to stress.

## Key facts

- **NIH application ID:** 10799065
- **Project number:** 2R01EY017863-14A1
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** JAMES Bryant HURLEY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $441,250
- **Award type:** 2
- **Project period:** 2007-09-15 → 2028-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10799065

## Citation

> US National Institutes of Health, RePORTER application 10799065, Control of Photoreceptor Metabolism (2R01EY017863-14A1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10799065. Licensed CC0.

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