The pancreas contains three different types of cells, each of which produces different hormones that contribute to the regulation of blood sugar levels, one way or another.
These cells are alpha-cells that produce glucagon to boost blood sugar, beta-cells that produce insulin to lower levels of glucagon, and delta-cells that produce somatostatin, a hormone that regulates alpha- and beta-cell activity.
In both type 1 and type 2 diabetes, research has linked the lack of insulin with problems in pancreatic beta-cells.
However, a new study by researchers from the University of Bergen in Norway suggests that, with just a small “push,” we may be able to train the body to start producing adequate levels of insulin once more, on its own.
More specifically, the investigators explain, some alpha-cells could turn into beta-cells and release insulin.
“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,” says study co-author Luiza Ghila from the Raeder Research Lab in the Department of Clinical Science at the University of Bergen.
The researchers explain their findings in detail in a study paper in the journal Nature Cell Biology.
‘Reprogramming’ cells to produce insulin
Each cell in the body develops to serve a particular function, but the “identity” that some cells take on is not always final, as the investigators in the current study note.
Instead, some adult cells are able to adapt and shift and can potentially replace cells with other functions that have died or become damaged.
“[Adult] cells are not terminally differentiated but maintain some plasticity potential even in higher organisms,” the researchers note.
Cells might change and adapt as a result of injury or stress to compensate for the loss of other, neighboring cells. However, scientists are still striving to gain a better understanding of how and when this happens, since this process has important potential in regenerative medicine.
In the current study, the researchers were able, for the first time, to uncover some of the key mechanisms that allow cells to “switch” identity, looking specifically at pancreatic alpha- and beta-cells in a mouse model.
They found that alpha-cells respond to complex signals they receive from neighboring cells in the context of beta-cell loss. Approximately 2 percent of alpha-cells can thus “reprogram” themselves and start producing insulin.
By using a compound able to influence cell signaling in the pancreas, the researchers could boost the number of insulin-making cells by 5 percent. While this may be a relatively small number, it is a significant first step in learning how to wield the body’s own potential to fight diabetes.
“If we gain more knowledge about the mechanisms behind this cell flexibility, then we could possibly [….] control the process and change more cells’ identities so that more insulin can be produced,” says Ghila.
Such findings, the investigators add, will help boost treatments, not just for metabolic diseases such as diabetes, but also for other conditions, including Alzheimer’s where the function of specific brain cells becomes impaired.
“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.”
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