Author(s): Luki Benavente
Mentor(s): Jeffery S. Tessem
Institution BYU
Diabetes is characterized by the inability of cells within the liver, muscle and fat to absorb glucose from the bloodstream due to beta cell failure or loss, and a corresponding reduction of insulin secretion. Experimental trials have shown that the transcription factor Nr4a3 is associated with beta cell function. When Nr4a3 is knocked out, a decrease in glucose-stimulated insulin secretion (GSIS) and a decrease in beta cell proliferation are observed. When Nr4a3 is overexpressed, an increase in beta cell proliferation is seen. Nr4a3 directly correlates to the beta cells’ ability to produce insulin, minimizing the hyperglycemic state resulting from beta cells failure. Identifying the binding partners of Nr4a3 that allows it to properly function will allow for a clearer understanding of how cells can be manipulated to continue to proliferate and secrete insulin. Here we identify binding partners of Nr4a3 that play a role in how Nr4a3 controls beta cell proliferation and insulin secretion. These results have significant effects on future research regarding how beta cells can continue to proliferate to maximize the output of insulin in the body. This data opens doors to the discovery of new proteins that could also be affecting the uprise in diabetes diagnosis because of beta cell failure and insulin depletion in the body.