# Insulin, a new role in retinal homeostasis and disease

> **NIH NIH F32** · UNIVERSITY OF VIRGINIA · 2021 · $72,630

## Abstract

Abstract
Different organs within our bodies have different energy requirements. Such requirements are influenced by
the particular function performed by the organ, and the body’s nutritional status. Moreover, energy use of one
organ is many times matched by a decrease in energy consumption of another. The liver, for example, will
decrease, and sometimes spend energy to support muscle function. However, the central nervous system
(CNS) needs to utilize adequate amounts of energy, irrespective of the body’s nutritional status or the
metabolic needs of other organs. How the CNS is able to obtain this “metabolic privilege” is unclear, yet deficits
in energy supply to the CNS often underlie diseases such as age-related macular degeneration (AMD) and
Alzheimer’s disease.
Insulin is the major anabolic hormone in the body. Primarily produced in the pancreas, insulin is released into
the blood upon the consumption of food. When sensed by cells in other parts of the body, insulin triggers a
cascade of signaling events that allow tissues to take up glucose from circulation. In the context of the retina,
insulin is important in homeostasis. Absence of insulin can lead to eye specific diseases such as diabetic
retinopathy. Yet how insulin regulates glucose metabolism in the retina is unclear. Crucial to glucose and
overall retinal metabolism is the retinal pigment epithelium (RPE). The RPE is a monolayer of pigmented cells
forming the blood retinal barrier and recent research has shown that the RPE regulates glucose transport from
the periphery into the retina. Preliminary studies in our lab have uncovered that the RPE mediates insulin
signaling in the retina. The purpose of this proposal therefore is to test the importance of RPE mediated insulin
signaling on glucose metabolism within the retina. We hypothesize that insulin, through the RPE, allows the
eyes to maintain an adequate supply of energy at all times, irrespective of nutritional status. Furthermore, we
hypothesize that failure in insulin signaling coming from this source can lead to problems in visual function,
including neovascularization and photoreceptor atrophy. To test this we will first measure what triggers RPE
mediated insulin signaling. We will then measure the impact that knocking out insulin has on glucose uptake by
the retina. Finally, we will analyze the downstream consequences that impaired RPE mediated insulin signaling
has on retina homeostasis and disease. The results of these studies could provide exciting new concepts on
the biology of the eye itself, energy utilization in the retina, and help develop new therapeutics to treat
blindness.

## Key facts

- **NIH application ID:** 10105192
- **Project number:** 5F32EY031211-02
- **Recipient organization:** UNIVERSITY OF VIRGINIA
- **Principal Investigator:** Jon Iker Etchegaray
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $72,630
- **Award type:** 5
- **Project period:** 2020-02-01 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10105192

## Citation

> US National Institutes of Health, RePORTER application 10105192, Insulin, a new role in retinal homeostasis and disease (5F32EY031211-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10105192. Licensed CC0.

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