A study highlights a new mechanism linking mitochondria, the energy power plants of our cells, to the dysfunctions of insulin producing cells in patients with type 2 diabetes.
- Researchers have discovered that dysfunctional mitochondria in pancreatic β cells trigger a response to stress, preventing their maturation and their production of insulin.
- This mechanism, also observed in liver cells and adipose, could explain type 2 diabetes.
- Good news: these cells do not die, which allowed scientists to test the Isrib, a molecule that blocks this response to stress. After four weeks, β cells have found their function, opening the way to new treatments.
Affecting hundreds of millions of people worldwide, type 2 diabetes is often associated with insulin production and use problems. A team of researchers from the University of Michigan, in the United States, has just highlighted a new mechanism linking mitochondria-cell energy power plants-to dysfunctions of insulin producing cells.
The role of mitochondria in insulin production
When the mitochondria is defective, their inability to produce enough energy can disrupt the functioning of cells, including β cells of the pancreas responsible for insulin production. Previous research had already shown that these cells have abnormal mitochondria in diabetic patients, but without explaining why.
In this new study published in the journal Sciencethe researchers identified a key process. Damage three essential components of mitochondria in mice, they observed that β cells activate a response to stress, leading to their immaturity and their inability to produce enough insulin. In other words, “The mitochondria send a signal to the cell nucleus which alters the destiny of the cells”summarize scientists in a press release. Note that they were able to confirm these results on human pancreatic cells, thus strengthening the relevance of their discovery.
Towards a treatment to restore the function of cells?
Diabetes is a complex disease that affects several organs. The research team therefore extended their experiences to liver cells and adipose cells. The same stress mechanism has been observed, confirming that mitochondria play a central role in the disease.
One of the most promising aspects of this study lies in the fact that affected cells do not die, but become dysfunctional. This observation led researchers to test a molecule, the ISRIB, capable of blocking the response to stress. After four weeks of treatment, β cells have regained their ability to regulate blood sugar in mice.
These works are opening a new path to treatments to restore cellular function rather than simply overcoming the loss of insulin producing cells. If these results are confirmed in humans, they could mark a major advance in the fight against type 2 diabetes, conclude the authors.
