Authors: Jakob Lenker, Trevor Kendrick
Mentors: Jeff Tessem
Insitution: Brigham Young University
Diabetes is characterized by a loss in beta cell function within the pancreas and the subsequent inability to produce sufficient insulin to regulate blood glucose. While current diabetes treatments focus on delivering pharmaceutical insulin to diabetic individuals, such treatments are temporary solutions and do not address the root of the issue. Instead, our research focuses on potential mechanisms for inducing greater insulin secretion within the pancreas of the individual. NK6 Homeobox 1 (Nkx6.1) is a major transcription factor in beta cells and its overexpression in beta cells is associated with higher insulin secretion. We have shown that Syntaxin 1A (Stx1A) interacts with Nkx6.1; Stx1A is of particular interest due to its role in mediating insulin granule fusion at the beta cell plasma membrane, directly impacting insulin secretion. We hypothesize that the interaction between Nkx6.1 and Stx1A may play an important yet understudied role in insulin secretion. Here, we present the results of Stx1A overexpression on glucose-stimulated insulin secretion within pancreatic beta cells, as well as the effect on the Nkx6.1 interaction. Understanding more about the role of Stx1A in beta cells could provide therapeutic targets to induce greater insulin secretion, which could aid in the effort toward finding a cure to diabetes.