Two new studies have shown how insulin-producing cells may fail in diabetes and how they might someday be restored.
The first study led by UC San Francisco (UCSF) scientists suggested that some cases of diabetes may be caused when beta cells are deprived of oxygen, prompting them to revert to a less mature state that renders them incapable of producing insulin.
The second study demonstrates that acinar cells, pancreatic cells that do not normally produce insulin, can be converted to functional beta cells, a potential new avenue for treating the disease.
In the first study, a gene known as VHL was selectively deleted from beta cells in mice. Insulin production in these beta cells was sharply reduced, and over time the mice developed the physiological equivalent of type 2 diabetes.
The team behind the first new study suggested that a decline in the function of beta cells over time may be a factor in many cases, such as in the subset of lean adults who develop diabetes.
During the development of the pancreas, changes in gene expression cause some cells to differentiate into beta cells, but when the researchers examined the VHL-deprived beta cells they found the cells had "de-differentiated."
In the second study, researchers were able to restore normal insulin and glucose levels in mice with no functional beta cells by transforming other pancreatic cells into "beta-like" cells.
In additional experiments the group showed that the cytokine treatment had exerted its effects by "reprogramming" acinar cells-pancreatic cells that normally secrete digestive enzymes rather than insulin-and causing them to take on the properties of beta cells, including glucose sensing and insulin secretion.
The studies were published in journal Nature Biotechnology and Genes 'n' Development.
