Type 2 diabetes (T2D) is a chronic condition that affects millions of people worldwide. T2D is characterized by hyperglycemia caused by inadequate pancreatic beta cell function. There are various ways to treat T2D such as insulin injections, dieting, exercise, and medication. Stimulating endogenous beta cell receptors that potentiate glucose stimulated insulin secretion (GSIS) could be harnessed as a therapy for T2D, such as is used with GLP-1. Adrenergic receptors are expressed on the beta cell, and potentiate glucose stimulated insulin secretion in vivo. Stimulation of adrenergic receptors induces cAMP. We have shown that forskolin treatment of Ins-1 beta cells increases cAMP levels and enhances Nr4a1 and Nr4a3 mRNA expression. The Nr4as have also been shown to enhance GSIS, however the relationship between the adrenergic receptors and Nr4as in relation to GSIS remains largely unexplored. In order to investigate this relationship we will conduct GSIS assays following adrenergic receptor stimulation in wild type, Nr4a1 knockout, and Nr4a 3 knockout mice. Here we present our findings on the effects of adrenergic receptor potentiated GSIS in Nr4a1 and Nr4a3 knockout Ins-1 beta cells and primary mouse islets.
University / Institution: Brigham Young University
Format: In Person
SESSION C (1:45-3:15PM)
Area of Research: Science & Technology
Faculty Mentor: Jeffery Tessem