Author(s): America Teare
Mentor(s): Jeffery S. Tessem
Institution BYU
Diabetes mellitus affects one in ten people worldwide, posing a major public health challenge. Both type I and type II diabetes are characterized by reduction of glucose-stimulated insulin secretion (GSIS) and β-cell mass. Although type I and type II diabetes have different underlying causes, restoring β-cell function and mass offers a potential treatment for both. Previous research has shown that the orphan nuclear receptor Nr4a1, a transcription factor, plays a role in cell proliferation and could be adapted as a possible treatment for diabetes. CDIM-PHCH3 (CDIM) is a compound that binds Nr4a1 and serves as an agonist, enhancing Nr4a1’s activity. We hypothesize that treatment of INS-1 cells with CDIM will enhance Nr4a1 expression, transcription of downstream targets, and β-cell proliferation. Here we present the effects of CDIM-PHCH3 agonism on the expression and transcriptional activity of Nr4a1, expression of downstream targets, and β-cell proliferation and glucose stimulated insulin secretion. The ability of CDIM-PHCH3 to potentiate Nr4a1 activity could potentially allow for its use to restore functional β-cell mass as a treatment for diabetes.