A new piece of the puzzle to explain how Type 1 Diabetes occurs and model the process in beta cells

A new study by CHRIM staff member and lead author Gabriel Brawerman in the lab of Dr. Peter Thompson has been published in the journal Molecular Metabolism.

The study, entitled “DNA damage to beta cells in culture recapitulates features of senescent beta cells that accumulate in type 1 diabetes” provided insights into how type 1 diabetes develops and explored new model systems to understand this process.

About the study:

Type 1 Diabetes (T1D) is a metabolic disorder that frequently affects children and youth and results from a poorly understood process whereby the immune system mistakenly attacks and destroys most of the insulin-producing beta cells in the body. Although most of the beta cells are lost in T1D, some beta cells survive and become dysfunctional. Dr. Thompson’s research team previously found that some of the survivor beta cells in people who develop T1D undergo a cell stress response called “senescence”. Senescent beta cells act like accelerants to the process of developing T1D, as removing these harmful cells prevents T1D in preclinical models. However, it remained to be determined why some beta cells become senescent.

In this study, Dr. Thompson’s team found that specifically triggering a damage response to the beta cell’s DNA leads to activation of the senescence program. This suggests that the reason that some beta cells become senescent during T1D is because they experience DNA damage that cannot be efficiently repaired. As part of the study, Dr. Thompson’s team developed the first human beta cell models of senescence during T1D, with the goal of further defining the key players in this response and developing safe and effective therapeutics.

“These studies help to explain a key piece of the puzzle as to how T1D develops from the perspective of the beta cells and takes us a step closer towards developing safe and effective therapies”.