Type 1 diabetes is caused by the loss of insulin-producing () cells in pancreas. A significant
advance in cell therapy for diabetes has been the development of a protocol for islet transplantation
from Dr. James Shapiro and colleagues at the University of Alberta in Edmonton, Canada (the
Edmonton protocol). However, lack of suitable organ donors for transplantation is a critical factor that
limits this therapy from majority of individuals suffering from diabetes. Research in the last decade has
therefore been largely focused on generating insulin-producing cells that can be easily obtained
(derived) and used in transplantation setting for replacement therapy in diabetes. Although insulinproducing
cells have been obtained from various sources including human ES cells, bone marrowderived
mesenchymal cells, umbilical cord-blood derived mesenchymal cells, transdifferentiation of
liver / gallbladder cells, pancreatic duct cells, exocrine cells as well as islet-derived mesenchymal cells,
the amount of insulin produced by most of these cell types is significantly less as compared to the
amount of insulin produced by a normal adult pancreas. Present research is therefore focused on
understanding signalling molecules and processes that would enhance differentiation of these cells.
Although embryonic pluripotent/stem cells may be limited due to ethical issues, adult tissue-derived
progenitor cells are believed to possess inherent traits that result in “commitment” to a particular
phenotype, demonstrated by their relatively restricted differentiation capacity. In this chapter, we
discuss the cell types that have been studied for replacement therapy in diabetes with specific reference
to their possibility for use in a clinical setting.
Keywords: Diabetes, embryonic stem cells, pancreas, beta cells, differentiation, pluripotency, induced
pluripotent stem cells.
