Tiny structures inside our cells may play a much bigger role in type 2 diabetes than scientists once thought.
New research suggests that when these structures, called mitochondria, become damaged, they can push important cells into a less mature state and stop them from doing their jobs properly.
Mitochondria are often called the powerhouses of cells because they help turn nutrients from food into usable energy. Almost every cell depends on them, so problems with mitochondria can affect many organs and body functions.
This may be especially important in type 2 diabetes, a common disease in which blood sugar stays too high. The condition develops when the body does not respond well to insulin, does not make enough insulin, or both.
Insulin is made by beta cells in the pancreas and helps move sugar from the blood into cells for energy. Scientists have long known that the mitochondria inside beta cells are often damaged in people with diabetes, but it has been unclear exactly how this damage causes the cells to fail.
Researchers at the University of Michigan investigated this question in a study published in the journal Science. Using mice, they examined what happened when they disrupted different systems that beta cells use to keep their mitochondria healthy.
The team studied mitochondrial DNA, the process cells use to remove damaged mitochondria, and another system involved in maintaining mitochondrial health. Although these systems work in different ways, damaging any of them produced a similar result.
The unhealthy mitochondria triggered a stress response inside the beta cells. Instead of immediately dying, the cells became less mature and lost some of the features they needed to produce insulin normally.
This finding could help explain why insulin production falls as type 2 diabetes develops. Lead author Dr. Emily M. Walker and colleagues found that mitochondrial damage was not simply reducing the cells’ energy supply; it was also changing the identity and behavior of the cells.
The researchers then asked whether the same problem could occur elsewhere in the body. They created similar mitochondrial problems in liver cells and fat cells and found that these cells also became less mature and lost normal functions.
That matters because type 2 diabetes involves much more than the pancreas. The liver can release too much sugar into the blood, fat tissue can become unhealthy, and other tissues may respond poorly to insulin.
Senior author Dr. Scott A. Soleimanpour said the results point to mitochondrial stress as a possible shared process behind problems in several organs. This could give researchers a broader way to understand how diabetes develops across the body.
One of the most encouraging findings was that the damaged beta cells were still alive. Because the cells had not been destroyed, the researchers tested whether their normal function could be restored.
They treated the mice with an experimental compound called ISRIB, which interferes with the stress response triggered by mitochondrial damage. After four weeks, the beta cells began producing insulin again and the animals’ blood sugar returned to normal levels.
The result does not mean that a treatment for people with type 2 diabetes is ready. The work was carried out in mice, and researchers still need to learn whether the same process can be safely targeted in human cells and patients.
Still, the study offers an important new direction. Instead of viewing failing beta cells as permanently lost, scientists may be able to find ways to help some damaged cells recover their mature state and begin working again.
The researchers now hope to study the process in greater detail and examine cells from people with diabetes. If the findings translate to humans, they could eventually support treatments aimed at repairing cell function rather than only controlling high blood sugar.
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