In a major breakthrough in diabetes research, scientists have now discovered that some pancreatic cells that normally secrete digestive enzymes can be converted to functional beta cells that produce insulin - a hormone that plays a key role in diabetes prevention.
A team of researchers from University of California San Francisco (UCSF) successfully transformed the pancreatic acinar cells in mice into 'beta-like' cells to restore normal insulin and glucose levels.
Led by Luc Baeyens, a post-doctoral fellow in the laboratory of Michael S. German, professor of medicine and associate director of the UCSF Diabetes Centre, the researchers for the first time demonstrated that acinar-to-beta cell reprogramming is possible in a living animal through pharmacological treatment.
The new research represents a promising approach to therapy for type 1 diabetes, or for cases of type 2 diabetes marked by beta cell dysfunction.
"Type 1 diabetes patients would greatly benefit from pharmacological therapies that create new beta cells, provided the current findings in mouse models could be translated into targets in human pancreas," Baeyens said in a paper published in the journal Nature Biotechnology.
In a different but related study led by Sapna Puri, a scientist in the laboratory of Matthias Hebrok, director of the UCSF Diabetes Centre, suggested that some cases of diabetes can 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 beta cell is a highly sophisticated cell that produces tremendous amounts of insulin in a tightly regulated way," said Hebrok.
"What we are unraveling here is a different way of looking at how diabetes occurs," said Hebrok.
"It's not that you're perfectly fine and then you're pre-diabetic and then you're diabetic and then your beta cells die. Instead it's a slippery slope where the beta cell function erodes over time," Hebrok added.