Downregulation of Glis3 in INS1 cells exposed to chronically elevated glucose contributes to glucotoxicity-associated β cell dysfunction.

Chronically elevated levels of glucose are deleterious to pancreatic β cells and contribute to β cell dysfunction, which is characterized by decreased insulin production and a loss of β cell identity. The Krüppel-like transcription factor, Glis3 has previously been shown to positively regulate insulin transcription and mutations within the Glis3 locus have been associated with the development of several pathologies including type 2 diabetes mellitus. In this report, we show that Glis3 is significantly downregulated at the transcriptional level in INS1 832/13 cells within hours of being subjected to high glucose concentrations and that diminished expression of Glis3 is at least partly attributable to increased oxidative stress.

Experience conducting a community-engaged student research project involving an underrepresented community: A reflective essay.

Recruiting racially and ethnically underrepresented participants into genetics research studies has been challenging. While many institutions have taken steps to address the inequity in genetics research, genetic counseling training programs have the chance to inspire students to engage with underrepresented communities through utilizing different research methodologies. These methodologies can help students focus on research projects that increase access to genetics services and improve clinical care.