Buenos Aires – A team of Argentine scientists has made a potentially significant breakthrough in diabetes research, identifying a novel mechanism that bolsters the resilience of pancreatic beta cells. The findings, published this week in Cell Death & Disease, could pave the way for new therapies aimed at slowing the progression of both type 1 and type 2 diabetes, conditions affecting an estimated 500 million people globally. Researchers at the National institute of Neuroscience (CONICET-AUSTRAL) have demonstrated that controlled exposure to inflammation may actually strengthen these critical insulin-producing cells.
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</p>A new mechanism that helps pancreatic beta cells – responsible for producing insulin – resist damage has been discovered by medical researchers in Argentina, potentially paving the way for innovative treatments for diabetes. The disease affects more than 500 million people worldwide, according to UPI.
Argentine Scientists Achieve Breakthrough in Diabetes Treatment by Strengthening Beta Cells
The discovery was made by a research team from the Immunology, Endocrinology, Diabetes and Metabolism Laboratory at the National Institute of Neuroscience (CONICET-AUSTRAL), led by scientist Marcelo J. Perón.
The team demonstrated that beta cells can be “trained to adapt to low levels of inflammation, giving them a greater capacity to withstand attacks that usually lead to their destruction.”
Diabetes develops when these cells are damaged or destroyed, either by an autoimmune attack in type 1 diabetes, or as a result of chronic stress, obesity, and high blood glucose in type 2 diabetes. However, the new study, published in the journal Cell Death & Disease, reveals for the first time that certain inflammatory factors – particularly the cytokine IL-1β – may play a dual role. While toxic at high doses, they can grant cells greater resistance when exposed to low concentrations, a biological phenomenon known as hormesis.
Speaking to United Press International, Perón explained that the team found beta cells to be highly sensitive to cytokines, but low-level exposure prepares the cells to confront higher levels without being destroyed.
He emphasized that scientists have long believed IL-1β was solely responsible for cell death, but the new findings demonstrate its physiological role in enabling cells to adapt to stress.
This scientific advancement builds on more than twenty years of research, including biochemical experiments led by researcher Carolina Sitola, who helped clarify the mechanisms by which beta cells function and respond to inflammatory damage. The discovery opens the door to developing new drugs that preserve the function of insulin-producing cells and slow the progression of the disease in people with both type 1 and type 2 diabetes.
Despite the promising results, Perón stressed that the research is still in its early stages and that clinical applications will require further studies. The team is currently working to identify the internal mechanisms that give beta cells greater resistance to stress, with the goal of finding potential drug targets that could lead to future treatments capable of changing the course of the disease globally.
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