Researchers say they may have found a way to use pancreatic cells to initiate a “totally new form of treatment for diabetes“.
Their findings lie within the different functions of cells and how they work within the body.
The pancreas has three types of cells, alpha, beta and delta which all have different functions to control blood glucose.
The alpha cells produce glucagon which increases blood glucose levels, beta cells produce insulin which decreases blood glucose levels, and the delta cells make somatostatin, which controls the regulation of both the alpha and beta cells. Glucagon, insulin and somatostatin are all hormones.
Type 1 diabetes develops when the beta cells, which produce insulin, get destroyed by the bodys immune system. In type 2 diabetes, insulin doesn’t work as efficiently as it should. Some people that have lived with type 2 diabetes for many years may also have decreased ability to produce insulin as well.
Now, a team from the University of Bergen (UiB) have discovered that glucagon-producing alpha cells in the pancreas can change their identity and start producing insulin instead.
Researcher Luiza Ghila from the UiBs Raeder Research Lab, Department of Clinical Science, said: “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.”
Only about 2% of the neighbouring cells in the pancreas could change identity, but during the study, researchers were able to increase that figure to 5%.
They did this by introducing a drug that encourages surrounding cells to send out a signal which kick-starts the changing process.
“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,” added Ghila.
“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.”
The findings have been published in the journal Nature Cell Biology.
