Argentine Scientists Make Important Progress in Diabetes Treatment

BUENOS AIRES, Dec. 4 Scientists in Argentina have uncovered a process that enables pancreatic beta cells, responsible for insulin production, to resist damage. This discovery could pave the way for innovative diabetes therapies, a condition affecting over 500 million individuals globally.

The breakthrough was achieved by the team at the Immuno-Endocrinology, Diabetes, and Metabolism Laboratory at CONICET-AUSTRAL, under the leadership of Marcelo J. Perone. Their research demonstrates that beta cells can adapt to moderate stress and survive assaults that would usually destroy them.

Diabetes occurs when beta cells are impaired or destroyed, preventing the body from generating sufficient insulin, the hormone that controls blood sugar. In Type 1 diabetes, the immune system attacks these cells, while in Type 2, prolonged stress from obesity, inflammation, and high blood sugar gradually harms them.

The significance of this study lies in its revelation that beta cells can be trained through exposure to low levels of inflammation, making them more resilient to severe stress. This finding lays the groundwork for treatments that could protect beta cells and slow disease progression. The research, published in Cell Death & Disease, suggests new approaches to safeguard beta cells and manage a disease with profound health and economic consequences worldwide.

Perones team has been investigating insulin-producing cell function for nearly two decades, previously identifying critical mechanisms linked to beta-cell dysfunction. Biochemical experiments conducted by CONICET fellow Carolina Stula advanced their understanding of how beta cells respond to damage.

Beta cells are particularly sensitive to inflammatory molecules such as interleukin-1 beta (IL-1). Perone explained that the abundance of IL-1 receptors on beta cells prompted the team to investigate its effects. Laboratory experiments revealed that while high doses are harmful, very low doses allow beta cells to develop resistance to otherwise lethal concentrations.

In essence, IL-1 acts like a protective agent at low levels: initial exposure helps the cells adapt and survive later encounters with high concentrations without dying. This phenomenon, known as hormesis, describes how low doses of a potentially harmful substance can produce beneficial effects, while higher doses remain toxic.

The study challenges the longstanding belief that IL-1 only causes beta-cell death, highlighting its physiological role in helping cells endure stressful conditions. Low doses of IL-1 can effectively shield insulin-producing cells from inflammation, creating opportunities for therapeutic interventions in both Type 1 and Type 2 diabetes.

Perone emphasized that these findings could lead to treatments that preserve beta-cell function, slow disease progression, enhance patients quality of life, and reduce healthcare costs. While the research is still in its early stages, the team is exploring the internal mechanisms that enhance beta-cell resistance to inflammatory stress, aiming to identify potential drug targets.

Author: Connor Blake