Norway: Diabetes Research Pancreas Cells Can Change Identity to Produce Insulin
Norwegian researchers have found that neighbour-cells can take over functions of damaged or missing insulin-producing cells in the pancreas. The discovery may lead to new treatments for diabetes.
Bergen/Norway — In collaboration with other international researchers, researchers at the University of Bergen 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. Researcher Luiza Ghila at the Raeder Research Lab, Department of Clinical Science, University of Bergen (UiB) stated that we 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. The results are published in Nature Cell Biology.
The researchers discovered that only about 2 % the neighbouring cells in the pancreas could change identity. However, even that amount makes the researchers optimistic about potential new treatment approaches. For the first time in history, researchers were able to describe the mechanisms behind the process of cell identity. It turns out that this is not at passive process, but is a result of signals from the surrounding cells. In the study, researchers were able to increase the number of insulin producing cells to 5 %, 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 discoveries is not only good news for diabetes treatment. 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 disease and cellular damage due to heart attacks.