Scientists have discovered that an amino acid called glutamine is essential for keeping the eye’s light-sensing cells healthy, offering a potential new way to protect vision.
The retina, located at the back of the eye, contains specialized cells called photoreceptors.
These cells capture light and send visual signals to the brain, making vision possible.
Because they are constantly working, photoreceptors have extremely high energy needs, which makes them vulnerable to even small disruptions in their metabolism.
When photoreceptors die, vision is lost—a common outcome in many retinal diseases. Currently, there are no treatments that can directly improve their survival.
Previous research has mainly focused on glucose as their main fuel source, and one glucose-based therapy is now being tested in clinical trials for people with retinal degeneration.
But researchers at the University of Michigan wanted to know whether photoreceptors also rely on other energy sources. “Photoreceptors are one of the most metabolically demanding cells in the body,” said Thomas Wubben, M.D., Ph.D., assistant professor of ophthalmology and visual sciences.
“We looked at glutamine because it is the most abundant amino acid in the blood.”
Glutamine is important for several cellular functions. It helps make other amino acids—such as glutamate and aspartate—as well as proteins and DNA.
To study its role in vision, the team used mice that lacked an enzyme called glutaminase, which is needed to convert glutamine into glutamate.
The results were striking: mice without glutaminase quickly lost retinal thickness and experienced a drop in both photoreceptor number and function. They also had much lower levels of glutamate and aspartate, which are essential for building the proteins that photoreceptors need to work properly.
The shortage of these amino acids also activated a cellular “stress response.” While this response can be protective in the short term, if it remains active for too long, it can trigger cell death. When the researchers used a treatment to block the stress response, the retinas of the mice became thicker again, suggesting some recovery.
These findings show that glutamine is vital for photoreceptor survival and that disruptions in its metabolism can contribute to vision loss. In fact, problems with the glutamine-to-glutamate pathway are already seen in models of human retinal disease.
The next step for Wubben and his team is to find out exactly which pathways depend on glutamine and whether they can be supported with drugs or nutritional supplements. “It is possible that resetting metabolism can help prevent vision loss and blindness,” Wubben said.
The study is published in the journal eLife.
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Source: University of Michigan.
