Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
Approximately 9.4 percent of the United States is affected by type 1 or type 2 diabetes. Diabetes results from the body’s inability to maintain healthy blood glucose levels due to the loss of pancreatic β-cells (insulin secreting cells) or from the body’s insulin sensitive cells becoming insulin resistant. Both type 1 and type 2 diabetes results in a loss of functional β-cells. The current treatments for diabetes are insulin injections or transplants, many times requiring up to three donors per transplant. Neither option is an optimal cure: insulin injections do not cure the disease, and transplants are not available to the majority of people. We propose that being able to replicate β-cells in-vivo would allow us to provide a cure to diabetes. β-cells stop reproducing (proliferating) soon after birth except in a few occasions such as obesity and pregnancy, leading us to believe that there are key gene(s) that induce cell proliferation when activated. Finding these gene(s) would present a viable cure, being able to grow β-cells in-vivo for transplantation or even injection. The gene MafA is present in mature β-cells and previous research has revealed its vital role in the pancreas. MafA is turned on around embryonic day 15.5 and steadily increases expression up until the cell becomes a mature β-cell. The time period when MafA is turned on corresponds with when a β-cell is proliferating and developing leading us to believe that MafA is crucial to finding a cure. Here we show the effect of MafA overexpression on INS1 832/13 β-cell proliferation, survival, and insulin secretion.