In order to determine the function of Follistatin Like-3 we created knockout mice in which the gene that codes for this protein was disabled. Mice without FSTL3 had larger pancreatic islets and improved glucose control suggesting that loss of FSTL3 might be beneficial for patients with diabetes. We continued our analysis of these mice and found that the increased number of insulin producing beta cells was not due to increased proliferation of the existing beta cell population.
Our current research is focused on whether loss of FSTL3 stimulates a process where other cell types in the pancreas, such as alpha cells, change their fate and become beta cells, a process known as transdifferentiation or reprogramming. Regardless of the actual mechanism, however, Fairbanks Pharmaceuticals is focused on development of new diabetes therapies based on altering FSTL3 function.