Scientists in Argentina have identified a mechanism that enables pancreatic beta cells, which produce insulin, to resist damage. The discovery could pave the way for new therapies for diabetes, a condition affecting more than 500 million people worldwide.
The breakthrough comes from the Immuno-Endocrinology, Diabetes and Metabolism Laboratory at CONICET-AUSTRAL, led by Marcelo J. Perone. The team found that beta cells can adapt to moderate stress, surviving attacks that would normally destroy them.
Diabetes arises when beta cells are damaged or destroyed, reducing the body’s ability to produce insulin, the hormone that regulates blood sugar. In Type 1 diabetes, an autoimmune response eliminates the cells, while in Type 2, chronic stress from obesity, inflammation, and high glucose gradually wears them down.
The study shows that beta cells can be “trained” with low levels of inflammation to withstand greater harm. This finding provides a foundation for therapies aimed at protecting these cells and slowing disease progression.
Published in Cell Death & Disease, the research demonstrates a potential strategy to preserve beta-cell function and manage a disease with significant global health and economic consequences.
Perone’s team has spent nearly two decades studying the mechanisms behind beta-cell dysfunction. Using biochemical experiments conducted by CONICET fellow Carolina Sétula, they advanced understanding of how these cells respond to stress.
Beta cells are highly sensitive to inflammatory molecules, especially interleukin-1 beta (IL-1β), whose levels spike during infections and inflammation. “For years, researchers believed IL-1β only caused beta-cell death,” Perone told UPI. “Now we see it also helps cells adapt under adverse conditions.”
Through in vitro experiments, the team discovered that IL-1β’s effect depends on its concentration. At high levels, it is toxic, but at low levels, it triggers an adaptive response that protects cells from future damage. This process, known as hormesis, allows cells to strengthen themselves against stress.
“Our study shows that low doses of IL-1β, once considered harmful, can protect insulin-producing cells from inflammation,” Perone said.
The discovery opens new possibilities for therapies that could preserve beta-cell function in both Type 1 and Type 2 diabetes, improving patients’ quality of life and potentially reducing healthcare costs.
Perone emphasized that the research is still in early stages. The team is now investigating the internal mechanisms that increase beta-cell resistance to inflammatory stress, aiming to identify targets for future drug development.
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