Researchers in the US find way to delete old cells and prevent the risk of developing type 2 diabetes.
DRWF-funded researchers in the US have found a way to restore the function of aged beta-cells – that could reduce insulin resistance and the risk of developing type 2 diabetes.
In studies carried out at the Joslin Diabetes Center, Boston, Massachusetts, researchers found that insulin resistance increased the proportion of aged beta-cells not working and could lead to the development of type 2 diabetes.
The results of the study were recently published in Cell Metabolism and confirmed a similarly increased proportion of aged beta-cells in islets recovered from humans with type 2 diabetes.
The study also showed that beta cell function could be recovered by removing these aged populations of beta cells either through genetic modification or oral medication.
Cristina Aguayo-Mazzucato, MD, PhD, Assistant Investigator in the Section on Islet Cell and Regenerative Biology and study author, said: “Our hypothesis was that there was an important component in the development of diabetes which consisted of accelerated aging of beta-cells and that this population could be targeted therapeutically.”
This research falls into a broader field of the study of senescence, the slow decline of the expansion and function of a specific cell population.
These cells grow larger as organisms get older, but certain circumstances can cause some cells in an organism to age faster than the whole.
Watch a video of Cristina Aguayo-Mazzucato, MD, PhD, talking about her research into the application of senolysis to the rejuvenation of beta-cell function in type 2 diabetes here:
Credit: Joslin Communications Office
Dr Aguayo-Mazzucato, who led the research team, said: “What we found is that indeed, insulin resistance was increasing the amount of senescent or old beta-cells.
“We were able to recover beta cell function, we were able to restore glucose tolerance.”
The ability to restore beta cell function with minimal intervention could be a game changer in the care of type 2 diabetes.
For many people living with the condition, beta cell function declines to the point where they need injectable insulin.
Researchers said they believed the implications for treatment “could be huge” following further clinical trials, with potential for reducing the risk or preventing type 1 diabetes.
Dr Aguayo-Mazzucato added: “When you look at the absolute percentage or quantity of the senescent beta-cells, they rarely exceed 20% of the whole beta cell population and yet targeting this relatively minor population had a huge effect on function and glucose metabolism and cellular identity.
“This opens a new target to treat diabetes which is basically to target populations of old or senescent cells that are really contributing to the local disfunction.
“In fact, it's a very exciting and rapidly growing field in medicine, which is called Senolytics or Senolysis.
“It has promises, as shown by other laboratories, in osteoarthritis, muscle frailty or degeneration, renal function, some brain function.
“What we're seeing is that senescence is, in reality, a response to stress. In the case of type two diabetes, this stress is insulin resistance. In the case of type 1 diabetes, it is the immune attack on beta-cells.
“But in both models, beta-cells are responding to these stresses by becoming senescent. So, we think that the potential of this new vision of preventing diabetes will be valid for both type 1 and type 2 diabetes.”
Senolysis, or the removal of aged or dysfunctional cells, is a growing field in the treatment of age-related health complications. This new research fits into the larger picture of how senolytics could help combat many different health complications of aging, leading to better quality of life.