Studies in mice, cells show link between glucose and oligodendrocytes
Written by Marisa Wexler, MS | May 4, 2026
- Brain sugar levels signal oligodendrocyte progenitor cells to divide or mature for myelin production.
- OPCs can use ketone bodies from fat breakdown to produce myelin if glucose is unavailable.
- Ketogenic diets restored myelin production in mice, suggesting new metabolic strategies for MS.
The amount of sugar in the brain plays a key role in governing the activity of oligodendrocytes, the brain cells responsible for making the protective myelin coating around nerve fibers, according to a study done in mice and cell models. The findings could have important implications for understanding diseases such as multiple sclerosis (MS), which is characterized by inflammation that damages myelin in the brain and spinal cord.
Researchers found that molecules derived from sugar are essential for the growth of immature cells that can develop into oligodendrocytes. When these cells can’t rely on sugar, they can make functional myelin using alternative metabolic sources, notably ketone bodies produced when the body burns fat.
In fact, myelin production was decreased in a genetically engineered mouse model in which oligodendrocytes could not use sugar, but these deficits were restored by feeding the mice a ketogenic diet — a high-fat, low-sugar diet designed to get the body to burn fat instead of sugar for energy.
“Our findings show that glucose is not just fuel for the brain, it’s also a signal for the cells to divide,” Sami Sauma, PhD, co-author of the study and postdoctoral research associate at the City University of New York (CUNY) Advanced Science Research Center, said in a university news story. “We found that when glucose levels are high in a particular brain region, progenitors use it to drive proliferation. As glucose levels shift, the same cells switch gears and begin maturing. It’s a beautifully coordinated metabolic system that helps shape brain development.”
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