Scientists have discovered a possible reason why insulin-producing cells stop working in type 2 diabetes, and the finding raises hope that some of this damage may be reversible.
The research from the University of Michigan focuses on mitochondria, tiny structures inside cells that help turn nutrients into usable energy.
Mitochondria are often called the powerhouses of cells because almost every organ depends on them for energy. When these structures become damaged, cells may struggle to perform their normal jobs, and mitochondrial problems have been linked to several diseases, including diabetes.
Type 2 diabetes develops when the body does not respond properly to insulin and eventually may struggle to produce enough of it. Insulin is a hormone that allows sugar from the bloodstream to enter cells, where it can be used for energy.
Much of the body’s insulin is produced by beta cells in the pancreas. These cells constantly monitor blood sugar and release insulin when levels rise, especially after a meal.
Scientists have known that mitochondria inside beta cells often do not work normally in people with diabetes. Until now, however, it has been difficult to understand whether mitochondrial damage simply accompanies diabetes or directly changes how these important cells behave.
The University of Michigan researchers used mice to investigate what happens when mitochondria in beta cells are deliberately disrupted. They examined several systems that mitochondria need to stay healthy, including their own DNA and the cellular machinery that identifies and removes damaged mitochondria.
The team found a similar result when different parts of these systems were disrupted. Damaged mitochondria triggered a stress response inside the beta cells, causing the cells to lose some of the mature features they need to make and release insulin properly.
In simple terms, the cells did not disappear, but they stopped acting like fully functioning insulin-producing cells. This loss of normal cell identity reduced insulin production and contributed to high blood sugar.
Lead author Dr. Emily M. Walker and colleagues also wanted to know whether this response was unique to the pancreas. Diabetes affects many organs, including the liver, muscles and body fat, so the researchers performed related experiments in liver cells and fat-storing cells.
They found a similar pattern. Mitochondrial problems activated stress signals that caused these cells to lose some of their normal functions, suggesting that the same basic process could affect several tissues involved in diabetes.
Senior author Dr. Scott A. Soleimanpour said this may help scientists understand why diabetes is such a whole-body disease. Problems with insulin production, liver sugar output, body fat and other metabolic processes may have some shared links to mitochondrial stress.
Perhaps the most encouraging finding was that the affected beta cells were still alive. Because the cells had not been permanently destroyed, the researchers tested whether blocking the harmful stress response could help them recover.
The team treated mice with an experimental compound called ISRIB, which interferes with the stress response activated after mitochondrial damage. After four weeks, the beta cells began producing insulin again and blood sugar levels in the mice returned to normal.
This does not mean that ISRIB is ready to treat people with type 2 diabetes. Results in mice do not always translate to humans, and researchers will need to establish whether the same process occurs in human diabetes and whether it can be targeted safely.
Still, the discovery offers an intriguing possibility: some cells that appear to have failed in diabetes may not be permanently lost. If scientists can find safe ways to restore their normal function, future treatments might address an underlying cause of the disease rather than only lowering blood sugar.
The University of Michigan study was published in the journal Science. The researchers are continuing to investigate the process and hope that studying human cells from people with diabetes will reveal whether restoring stressed cells could eventually become a practical treatment strategy.
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