Argentine Scientists Identify Mechanism That Protects Insulin-Producing Cells
BUENOS AIRES, Argentina — December 4, 2025 — Researchers in Argentina have uncovered a biological mechanism that enables pancreatic beta cells, responsible for insulin production, to resist damage. This breakthrough could pave the way for novel treatments aimed at preserving beta cell function in diabetes, a condition affecting over 500 million people globally.
The study was conducted by a team at the Immuno-Endocrinology, Diabetes and Metabolism Laboratory at CONICET-AUSTRAL, led by Marcelo J. Perone. Their research demonstrated that beta cells can adapt to moderate stress and survive assaults that would typically destroy them.
Diabetes arises when beta cells are damaged or destroyed, impairing the body’s ability to produce sufficient insulin, the hormone that regulates blood sugar. In Type 1 diabetes, an autoimmune response eliminates these cells, while in Type 2 diabetes, factors such as obesity, chronic inflammation, and elevated glucose levels gradually impair their function.
The researchers found that exposing beta cells to low levels of the inflammatory molecule interleukin-1 beta (IL-1β) enables the cells to develop resistance to higher, normally harmful concentrations. This process, known as hormesis, involves a low dose of a potentially damaging agent triggering a beneficial adaptive response.
“Our experiments showed that while high levels of IL-1β are toxic to beta cells, low doses act like a vaccine, training the cells to withstand subsequent higher doses without dying,” Perone explained. This finding challenges the previous belief that IL-1β solely causes beta cell death, revealing its role in helping cells adapt under stress.
The study, published in the journal Cell Death & Disease, builds on nearly two decades of research by Perone’s team, including biochemical experiments led by CONICET fellow Carolina Sétula. Their work advances understanding of beta cell function and response to damage.
Perone noted that the discovery opens possibilities for developing therapies that protect beta cells and slow diabetes progression, potentially improving quality of life and reducing healthcare costs. However, he emphasized that the research is in early stages and clinical applications will require further investigation.
Currently, the team is exploring the internal mechanisms that enhance beta cell resistance to inflammatory stress to identify potential drug targets. This research offers a promising foundation for future interventions aimed at preserving insulin-producing cells in both Type 1 and Type 2 diabetes.
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