Skip to main content
Utah's Foremost Platform for Undergraduate Research Presentation
2021 Abstracts

Downstream Targets of Nkx6.1 and Pdx1 Present Targets for Inducing Beta-Cell Proliferation

Presenter: Daelin Jensen, College of Life Sciences, Plant and Wildlife Sciences
Authors: Daelin Jensen, Connor Littlefield
Faculty Advisor: Jeffery Tessem, College of Life Sciences, Nutrition, Dietetics and Food Science
Institution: Brigham Young University

The global prevalence of diabetes is growing at an alarming rate. Both type 1 and type 2 diabetes are characterized by beta-cell death and a resulting decrease in beta-cell mass. Restoration of this lost beta-cell mass is key to curing diabetes and can be accomplished through the induction of beta-cell proliferation. We have shown that overexpression of the transcription factor Nkx6.1 is sufficient to induce beta-cell proliferation in young rat islets but not aged rat islets. We suspect this may be due to an altered binding interaction between Nkx6.1 and another beta-cell protein necessary for gene regulation. We have shown that Nkx6.1 binds to Pdx1, a second beta-cell specific transcription factor known to affect proliferation. These results suggest that Nkx6.1 and Pdx1 co-regulate a set of genes involved in beta-cell proliferation. However, this gene set has yet to be discovered. We hypothesize that Nkx6.1 and Pdx1 directly bind and co-regulate a set of genes involved in beta-cell proliferation. Using existing microarray data on genes affected by the overexpression of Nkx6.1 and Pdx1 separately, we have identified a gene set co-regulated by Nkx6.1 and Pdx1. The identification of this gene set presents several therapeutic targets to induce beta-cell proliferation in young and aged pancreata.