Washington: Diabetes is caused by the insulin cells’ inability to produce insulin; a hormone that is necessary is regulating blood sugar levels. Diabetics usually have to take insulin supplements to regulate these levels in their body.
Now, a study, headed by researchers at the University of Bergen, in collaboration with other international researchers, have discovered that glucagon producing cells in the pancreas, can change identity and adapt so that they do the job for their neighbouring damaged or missing insulin cells.
Speaking about the study, researcher Luiza Ghila at the Raeder Research Lab, Department of Clinical Science, University of Bergen (UiB) said that they are possibly facing the start of a totally new form of treatment for diabetes, where the body can produce its own insulin, with some start-up help.
According to the researchers, only about 2 per cent the neighbouring cells in the pancreas could change identity. However, even with that miniscule amount, researchers are optimistic about potential new treatment approaches.
Experts say that this was the first time in history that researchers were able to describe the mechanism behind the process of cell identity. It turns out that it is not a passive process but rather a result of signals from surrounding cells.
In the study, researchers were able to increase the number of insulin producing cells to 5 per cent, by using a drug that influenced the inter-cell signalling process. Thus far, the results have only been shown in animal models.
“If we gain more knowledge about the mechanisms behind this cell flexibility, then we could possibly be able to control the process and change more cells’ identities so that more insulin can be produced,” Ghila explains.
According to the researchers, the new discovery is not only good news for diabetes treatment but the cells´ ability to change identity and function, may be a decisive discovery in treating other diseases caused by cell death, such as Alzheimer´s and cellular damage due to heart attacks.
[source_without_link]ANI[/source_without_link]