In people with type 1 diabetes, blood sugar rises due to a loss of the insulin-producing pancreatic beta cells. Insulin is a hormone that helps the body use glucose for energy.

“One of the most interesting characteristics of these [adult] progenitor cells is that they are almost indistinguishable from embryonic progenitor cells,” said Harry Heimberg at the Juvenile Diabetes Research Foundation Center at Vrije Universiteit Brussel in Belgium and the Beta Cell Biology Consortium. “In terms of their structure and gene expression, there are no major differences. They look and behave just like embryonic beta cell progenitors."

“We at JDRF believe that this new research provides novel insights that may provide therapeutic potential to regenerate beta cells in type 1 diabetes,” said Patricia Kilian, Regeneration Program Director at JDRF.

Previous studies have suggested the existence of a beta cell progenitor in the pancreas after birth, but the identification and characterization of the progenitor cell has not been fully achieved. Other studies showing that replication of adult beta cells can account for beta cell turnover and expansion of beta cells under normal physiologic conditions and called into question the role or existence of a progenitor cell in regeneration. “Most people gave up looking because the cells are so few and so hard to activate,” added Heimberg.

In the new study, Heimberg’s team tied off a duct that drains digestive enzymes from the pancreas, a manipulation that led to a doubling of beta cell mass in the injured part of the pancreas within two weeks. The animals’ pancreases also began producing more insulin, evidence that the new beta cells were fully functional. Using a genetic labeling technique, the researchers found that the new beta cells were derived from precursor cells that expressed a gene expressed in embryonic progenitor cells called Neurogenin 3 (Ngn3) and that production of the new beta cells depended on activity of this gene. He suspects the regenerative process is sparked by an inflammatory response in the enzyme-flooded pancreas.

“The most important challenge now is to extrapolate our findings to patients with diabetes,” Heimberg reported. Although he cautioned that any potential diabetes treatment remains in the future, he said “our findings reveal the significance of investigating the feasibility of both isolating facultative beta cell progenitors and newly formed beta cells from human pancreas in order to expand and differentiate them in vitro and transplant them in diabetic patients and also composing a mix of factors able to activate beta cell progenitors to expand and differentiate in situ in patients with an absolute or relative deficiency in insulin.” -Juvenile Diabetes Research Foundation International