Beta Cell Refresh Halts Type 1 Diabetes Progression in Mice

In a new study, researchers were able to halt the development of type 1 diabetes in a mouse model by increasing proliferation and turnover of beta cells before signs of the disease even emerged. Their findings were published today in Nature Metabolism.

The remarkable findings were the result of experiments done by scientists at Joslin Diabetes Center in two different models of diabetes-prone mice. The first was a genetically engineered model that showed increased beta cell growth soon after birth, while the second was injected at an early age with an agent known to increase beta cell proliferation.

Samples collected from the spleen, showed an increase in T_reg cells capable of curbing an autoimmune response to β cells in the pancreatic islet and an overall reduction in β cell killing. When islet cells were transplanted from the protected animals to a different mouse, the recipient mouse was protected from the autoimmune reaction for a longer time.

"Even [in a highly susceptible mouse model], when you push the proliferation to generate new beta cells, 99 percent of the animals survived--and almost up to two years, which is very unusual," said Principal Investigator Rohit N. Kulkarni MD PhD, HMS Professor of Medicine and Co-Section Head of Islet and Regenerative Biology in the Joslin Diabetes Center.

Though the mechanism for this protection is still not entirely clear, it appears that something about the rapid turnover of the beta cells causes the beta cells to become “confused”. They no longer present autoantibodies typical of type 1 diabetes and seem to be more resistant to stress.

Further research is required to better understand the mechanism by which beta cell proliferation lowers autoimmunity typical of type 1 diabetes. Once that is done, it could be possible to move on to human studies and clinical trials.