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New Study Shows Glutamine's Importance for Retinal Health
Last reviewed: 09.08.2025
The retina places high energy demands on the body, partly due to the activity of the photoreceptors.
These specialized cells are responsible for receiving light and transmitting visual information to the brain.
Photoreceptor death is the cause of vision loss in many retinal diseases, and there are no effective therapies to enhance their survival.
In a paper published in eLife, researchers from the University of Michigan studied the glutamine dependence of photoreceptors. Their findings suggest that maintaining amino acid balance in these cells is important for photoreceptor health.
The energy requirements of photoreceptors make them vulnerable to minor changes in metabolism. Previous studies have focused on glucose as the primary fuel source for these cells.
A therapy that exploits the glucose dependence of photoreceptors is currently being tested in a clinical trial in patients with retinal degeneration.
“Photoreceptors are some of the most metabolically demanding cells in the body, which led us to wonder whether they depend on energy sources other than glucose for survival,” said Thomas Wubben, MD, PhD, associate professor of ophthalmology and visual sciences. “We looked at glutamine because it’s the most abundant amino acid in the blood.”
Glutamine is involved in several pathways, helping cells synthesize other amino acids, including glutamate and aspartate, as well as proteins and DNA.
To confirm glutamine's role in vision, the researchers used mice lacking the enzyme glutaminase, which breaks down glutamine into glutamate. They compared these mice to a control group by measuring the thickness of their retinas. The mice lacking glutaminase showed a rapid decrease in retinal thickness, with a loss of photoreceptor number and function.
Glutamine is involved in a variety of cellular processes. To understand why it is important for photoreceptor survival, the team measured levels of various molecules in control mice and in mice lacking glutaminase.
Mice without the enzyme had reduced levels of glutamate and aspartate. These amino acids, in turn, help cells synthesize proteins needed for photoreceptor function.
The researchers also found that reducing amino acid levels activated the integrated stress response, which is known to trigger cell death if it remains active for too long. When they suppressed the stress response, the team saw an increase in retinal thickness.
"We're now focused on understanding which pathways are dependent on glutamine and whether they can be 'switched on' with drugs or supplements," Wubben said.
Pathways converting glutamine to glutamate are disrupted in human retinal disease models.
"Restoring metabolism may help prevent vision loss and blindness."