14 DAY TRIAL // One of the primary issues with diabetes is that beta cells in the pancreas – which play a critical role in the production of insulin – are damaged irretrievably. In a new investigation, experts were able to uncover the mechanisms that lead to the development of such cells.
With this remarkable breakthrough, it may soon be possible to develop therapies and treatments against this condition, which currently affects millions of people around the world. The new approaches could either restore or increase beta cell function in patients suffering from type 1 diabetes.
This investigation was carried out by researchers at the Hebrew University of Jerusalem, in Israel, who were led by professor Yuval Dor at the university's Institute for Medical Research Israel-Canada.
The multi-year research effort also included researchers from the Hadassah University Medical Center and the diabetes section of the Roche pharmaceuticals company. The experts published details of their research in a recent issue of the scientific journal Cell Metabolism.
They explain that type 1 diabetes causes the body's immune system to believe that insulin-producing cells in the pancreas are invaders. This triggers an attack on these cells, which gradually lose their ability to synthesize insulin. Without the hormone, blood sugar levels cannot be controlled.
Accumulating glucose from the bloodstream is a critical function of metabolism. Without this chemical, cells cannot get their energy, and begin to starve, leading to a cascade of failures throughout the body, AlphaGalileo reports.
“Our work shows that as the glucose level is increased in the blood, it tells the beta cells to regenerate. It’s not blood glucose per se that is the signal, but the glucose-sensing capacity of the beta cell that’s the key for regeneration,” Dor explains.
According to the new investigation, the trigger can cause beta cells to regenerate, leading precisely to a high concentration of glucose in the bloodstream. The increase of beta cell replication and mass is one of the main avenues of research for treating this condition, so the new work will be very important in this regard.
The study shows “that the more work that beta cells are required to do (that is, the more ‘stressed’ they are), the more of themselves they make,” HUJ graduate student Shay Porat explains. He conducted the new study with fellow graduate student Noa Weinberg.
Their work was sponsored by a grant from the Juvenile Diabetes Research Foundation (JDRF). The investigation was carried out on mice, in which 80 percent of beta cells were destroyed intentionally. The researchers then analyzed how the cells responded to the stress they were being subjected to.