Presenter: Peter Ellsworth, College of Life Sciences, Plant and Wildlife Sciences
Authors: Drake Watkins, Haokun Yang, Jeffery S. Tessem
Faculty Advisor: Jeffery Tessem, College of Life Sciences, Nutrition, Dietetics, and Food Science
Institution: Brigham Young University
Diabetes is characterized as a chronic disease involving a decrease in insulin secretion and absorption, primarily due to a loss of beta cell function. Diabetes is impeding the lives of millions of people worldwide, giving way for researchers to rapidly search for pathways responsible for disease progression in beta cells. Several of these pathways revolve around a member of the nuclear receptor family 4a, Nr4a3. Nr4a3 drives insulin secretion and glucose absorption in the body. Global knockout (KO) of Nr4a3 decrease beta cell mass and proliferation. However, in other studies, increased Nr4a3 decreases insulin secretion. To clarify the dispute between these two opposing claims, we are studying the effects of Nr4a3 in a diabetic mouse model. Using global Nr4a3 KO mice, we present data regarding the loss of Nr4a3 on beta cell function through glucose stimulated insulin secretion (GSIS) and glucose tolerance tests (GTT). We further present data on the effects of Nr4a3 overexpression in the Ins-1 beta cell line on beta cell function.