Presenter: Kristopher Wieland, College of Life Sciences, Nutrition
Authors: Kristopher Wieland, Jefferey Tessem
Faculty Advisor: Jefferey Tessem, Life Sciences, Nutrition
Institution: Brigham Young University
About 10% of the U.S population suffers from the effects of type two diabetes (T2D). There have been methods created for treating its symptoms, but an overarching cure has yet to be established. T2D is characterized by beta cell desensitization to glucose and impaired glucose stimulated insulin secretion (GSIS). Research indicates that the transcription factor Nkx6.1 plays a large role in maintaining proper beta cell growth and insulin secretion. Exposure of beta cells to high concentrations of glucose (glucotoxicity) results in decreased Nkx6.1 expression and impaired GSIS. We present results demonstrating the effects of Nkx6.1 overexpression on beta cell glucotoxicity and insulin secretion. We demonstrate the effects of glucotoxicity on Nkx6.1 and target gene expression and GSIS, and the ability of Nkx6.1 overexpression to restore beta cell functionality under glucotoxic conditions. This research is an essential step in developing gene therapies for T2D by providing insight into the molecular mechanisms by which beta cells GSIS can be restored.