Authors: Jared Wieland, Jacob Herring
Mentors: Jeffery Tessem
Insitution: Brigham Young University
A central attribute of Type 2 Diabetes (T2D) is beta cell damage. This damage commonly affects beta cell’s ability to secrete insulin and regulate blood glucose levels. Nkx6.1 is a beta cell transcription factor essential for proliferation, differentiation, and glucose-stimulated insulin secretion. Hyperglycemia is detrimental to beta cell function and function. We hypothesize that hyperglycemia may negatively affect the expression and activity of beta cell transcription factors, including Nkx6.1. To provide an understanding of the effects of hyperglycemic conditions on Nkx6.1 expression, INS-1 832/13 beta cells were cultured in hyperglycemic conditions, then primary rat islets were treated for the same durations of time. Here, we present transcriptional, translational, cellular localization, and degradation of states of Nkx6.1 over 48 hours of hyperglycemic culture conditions both in vitro and ex vivo models. Comprehension of the mechanisms involved in hyperglycemic downregulation of Nkx6.1 is imperative to the development of treatments for diabetes.