Researchers at the University of Pittsburgh School of Medicine have successfully induced human insulin-producing cells, known as beta cells, to replicate robustly in a living animal, as well as in the lab.
The discovery not only could improve models and methods for studying diabetes, but also opens up new possibilities for treating the condition.
"Most scientists thought that these important pancreatic cells could not be induced to regenerate, or could only replicate very slowly," explained senior author Andrew F. Stewart, M.D., professor of medicine and chief of the Division of Endocrinology and Metabolism at the University of Pittsburgh School of Medicine. "This work provides proof-of-principle that the production of human beta cells can be stimulated, and that the newly generated cells function effectively both in the lab and in a living animal."
The findings are in the early online version of Diabetes , one of the journals of the American Diabetes Association.
Lead authors Nathalie Fiaschi-Taesch, Ph.D., assistant professor in Pitt's endocrinology division, and Todd A. Bigatel, M.D., a graduate of the postdoctoral fellowship program, identified molecules that play key roles in human beta, or islet, cell replication, building on previous work conducted by co-author Irene Cozar-Castellano, Ph.D., also an instructor of endocrinology, who performed similar studies using mouse cells.
They found that, unlike rodents, human beta cells contain a significant amount of a protein called cdk-6. When cdk-6 production was increased using a viral vector carrying the cdk-6 gene, the cells replicated. Stimulation was further enhanced by increasing production of another cell cycle molecule called cyclin D1. Untreated human islets did not replicate.