Authors: Owen Damitz
Mentors: Jeffrey Tessem
Insitution: Brigham Young University
Type one and two diabetes affect the everyday lives of millions of people worldwide. These diseases are characterized by decreased functional beta cell mass. Functional beta cell mass is defined by the beta cell’s ability to proliferate, secrete insulin, and resist apoptosis. We
have shown that the orphan nuclear receptor Nr4a3 is sufficient to induce beta cell proliferation. We have sought to define compounds that can interact with and modulate Nr4a3 activity. Using AutoDock Vina we have defined a number of compounds that interact with Nr4a3. Here we
present data demonstrating the ability of these compounds to modulate Nr4a3 mediated proliferation, survival, and insulin secretion in the beta cell. Furthermore, we demonstrate the effect of these compounds to modulate Nr4a3 transcriptional control. These findings are the basis for developing interventions to increase functional beta cell mass as a treatment for type 1 and type 2 diabetes.