Diabetes Mellitus is a chronic condition that affects millions of people worldwide. The main cause of diabetes is a reduced viable beta cell mass, the basis for this being reduced proliferation, increased cell death, and a decrease in glucose stimulated insulin secretion. Proper beta cell function is reliant on the transcription factor Nr4a1. Loss of Nr4a1 leads to a reduction in Beta cell proliferation and glucose stimulated insulin secretion. Not only do patients with type 2 diabetes exhibit a loss of viable beta cell mass, they also show a decreased expression of Nr4a1. Recent studies have shown that Nr4a1 binds to unsaturated fatty acids. We have shown that this binding reduces Nr4a1 transcriptional activity and cellular localization. We hypothesized that Nr4a1's ability to bind to its response element, NBRE, is impaired by the same fatty acids that are prevalent in type 2 diabetes. In order to test this hypothesis, we used an electrophoretic mobility shift assay (EMSA), which uses a fluorescently labeled DNA to determine Nr4a1-DNA interactions. We ran the EMSA in the presence of Fatty acids and observed the change they had on the band noting the effects carbon chain length and degree of unsaturation had on the band. Here we present the results of our studies.