Washington, June 2 : Scientists at UT Southwestern Medical Center have achieved a significant success in regenerating pancreatic beta cells in mice after inducing them to die.
Genetic engineering was the key to their success, said the researchers.
They said that the regenerative ability of their new animal model, the PANIC-ATTAC mouse, might provide future insights into improved treatments of diabetes.
According to them, the animal model mimics what occurs in humans with type 1 diabetes, a condition that develops when the body's immune system destroys pancreatic beta cells, as well as in type 2 diabetes, where beta cells die from working overtime.
During the course of study, the researchers first induced death in the beta cells, which make and release the hormone insulin, and found that the engineered mice's beta-cell populations could regenerate.
The group said that the finding was an indication that the animal was useful for studying conditions like type 1 diabetes, hyperglycemia (high blood sugar) and gestational diabetes.
"The ability to induce cell death is not novel. The fact that the beta cells regenerate after we kill them is really the new aspect of the model," said Dr. Philipp Scherer, professor of internal medicine, director of the Touchstone Center for Diabetes Research at UT Southwestern and senior author of the study.
"It enables us to see what kind of event or pharmacological intervention might stimulate or enhance the regeneration," he added.
Describing their study in the online edition of the journal Diabetes, the researchers said that they genetically manipulated mature, insulin-positive pancreatic beta cells in the PANIC-ATTAC mice so that the cells would die when they came in contact with a drug.
As the administration of the drug was stopped, it allowed the animals to recover.
The researchers observed that the animals' beta cells had regenerated, and their blood glucose levels returned to normal after two months.
Dr. Scherer admitted that it was yet unknown what caused the pancreatic beta cells to regenerate, but insisted that uncovering the mechanisms that allowed beta cells to rebound in that environment could provide major insights in type 1 diabetes research.
He also revealed that his team was contemplating developing way to isolate the cell population that would give rise to the newly emerging beta cells.
Dr. Zhao Wang, a postdoctoral researcher at UT Southwestern and lead author of the study, said the strength of the PANIC-ATTAC mouse as a research tool lies partly in the ability to test how specific pharmaceuticals impact beta-cell regeneration.
"We can test which drugs can more rapidly repair the damage. We can also test which drugs are protective. That's probably more important physiologically because it allows us to screen for interventions that could protect beta cells during the early stages of diabetes to slow down and prevent the onset of hyperglycemia," Dr. Wang said.