Researchers came a step closer to finding an effective treatment for type 1 diabetes using human embryonic cells.
These cells have allowed researchers to produce large quantities of human insulin-producing beta cells that can be used for transplantation, Harvard University reported.
"We are now just one pre-clinical step away from the finish line," researchers Doug Melton, whose daughter Emma also has type 1 diabetes.
Type 1 diabetes is an autoimmune metabolic condition in which the body attacks insulin-producing pancreatic beta cells, reducing the body's ability to regulate glucose. This new treatment would protect the beta cells from the immune system.
"For decades, researchers have tried to generate human pancreatic beta cells that could be cultured and passaged long term under conditions where they produce insulin. Melton and his colleagues have now overcome this hurdle and opened the door for drug discovery and transplantation therapy in diabetes," said Elaine Fuchs the Rebecca C. Lancefield Professor at Rockefeller University.
The process would require 150 million cells be transplanted into the body. Cell transplantation is still a relatively experimental treatment, and has only been used on a small number of patients. The device the researchers are working on proved to protect beta cells implanted in mice from immune attack for a number of months.
"[The new work is] an incredibly important advance for diabetes. There is no question that ability to generate glucose-responsive, human beta cells through controlled differentiation of stem cells will accelerate the development of new therapeutics. In particular, this advance opens to doors to an essentially limitless supply of tissue for diabetic patients awaiting cell therapy," said Daniel G. Anderson, the Samuel A. Goldblith Professor of Applied Biology, Associate Professor in the Department of Chemical Engineering, the Institute of Medical Engineering and Science, and the Koch Institute at MIT.
The research was published in a recent edition of the journal Cell.