Finding ways to reduce or eliminate the burden of injected insulin therapy for people with type 1 diabetes, and some with type 2 diabetes, is an important goal of diabetes research. One approach to eliminating the dependency on injected insulin is to replenish a person’s insulin-producing beta cells. Stem cells or other types of cells that could be reprogrammed to produce insulin may represent a good source of replacement tissue, but to tap their potential it is critical to understand the developmental program that creates a functional beta cell. New research uncovered a key factor necessary for making insulin-producing beta cells in both humans and mice. Previous research had identified a protein that helps trigger embryonic development of pancreatic islets, which contain beta cells and other cell types. Scientists now have found another key protein needed for the subsequent development of distinct islet cell subtypes. Mice lacking the newly identified protein—called Rfx6—can make islets, but these islets do not contain insulin-producing cells. They also fail to make some other hormones normally made by the pancreas. Interestingly, the scientists also found that a rare form of neonatal diabetes is associated with mutations in the human gene that produces the Rfx6 protein, suggesting that Rfx6 plays a critical role in beta cell development in humans as well as mice. Researchers therefore now know they will have to ensure that Rfx6 is present in order to successfully generate beta cells from some other cell type for transplantation into people with diabetes.
Smith SB, Qu H-Q, Taleb N, et al. Rfx6 directs islet formation and insulin production in mice and humans. Nature 463: 775-780, 2010.