To be or not to be... a pancreatic beta cell
Our genes are like a recipe for a human. It's a very complicated recipe, determining how much of this protein and how much of that enzyme need to be added into the mix in order for us to function properly, but our genes are pretty good at getting it right. Although we are still learning how the recipe works, what ingredients (gene products) are involved, and when are they are produced, our knowledge is growing fast.
For example, a master regulator gene has been identified that tells an embryonic cell whether or not to become a pancreas cell. Dr. James Wells and his team at the University of Cincinnati College of Medicine have determined that a gene called Sox17 acts like a toggle switch in mouse embryonic development. "In normal embryonic development, when you have an undecided cell, if Sox17 goes one way the cell becomes part of the biliary system. If it goes the other way, the cell becomes part of the pancreas," said Dr. Wells in a press release from Cincinnati Children's Hospital Medical Center. The results of Dr. Wells' study were published in the July 21 issue of Developmental Cell.
Dr. Wells and his colleagues are hoping that because Sox17 can tell undecided embryonic cells whether or not to become pancreatic tissue, it might also be able to tell stem cells (cells that can become almost anything in the body) to become pancreatic beta cells. If we could induce a cell to become an insulin-producing beta cell, we would be one step closer to treating and possibly curing type 1 diabetes. When the immune system attacks the beta cells in type 1 diabetes, it is often the case that most beta cells are destroyed before the disease has even been diagnosed. So creating new beta cells, possibly in a laboratory dish, and implanting them in patients is one possibility for treatment.
Preventing beta cell destruction in the first place is another avenue of research that is underway, and genes that are involved in protecting beta cells from the immune system are being studied as well.
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