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2021 Abstracts

Effects of TMAO on Beta-cell Apoptosis

Presenter: Jordan Davis, College of Life Sciences, Physiology and Developmental Biology
Authors: Jeffery Tessem, Emily Orton, Joseph Beales, Kacie Russon, Jordan Davis
Faculty Advisor: Jeffery Tessem, College of Life Sciences, Nutrition Dietetics and Food Science
Institution: Brigham Young University

The incidence of diabetes (DM) is growing worldwide, affecting 34.2 million people in the United States as of 2020. DM inhibits blood glucose homeostasis by reducing functional pancreatic ß-cell mass. In type 2 diabetes (T2D) this loss is associated with insulin resistance and is linked to chronic diseases, including obesity and cardiovascular disease (CVD). Clinical research shows that trimethylamine N-oxide (TMAO), a dietary gut metabolite known to be deleterious in CVD, is also elevated in T2D. However, TMAO’s effects on the ß-cell are unknown. In a cell culture model of T2D, glucolipotoxicity (GLT) treatment, we hypothesized that prolonged TMAO exposure would induce apoptosis more than the GLT alone and cause a worsened disease state. Here we present the effects of GLT with or without TMAO on ß-cell survival and induction of apoptosis. This research investigates a molecular rational for the association between T2D and CVD with the aim of identifying possible targets for novel treatment therapies.