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2018 Abstracts

Does NeuroD Enhance Functional Beta cell mass?

Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University

Diabetes affects over 30 million Americans and 422 million people worldwide. This disease impacts the body’s ability to produce insulin in response to glucose due to a loss of pancreatic β-cells. Type 1 and type 2 diabetes both result in a decrease of functional β-cell mass, which is characterized by effective secretion of insulin in response to glucose stimulation, the maintenance of β-cell survival, and the ability to cause β-cell proliferation. Currently, the answer for diabetics is to receive insulin injections or a donor pancreas or islet cells, neither of which successfully resolve the problem but are temporary fixes. Soon after birth, β-cell proliferation decreases significantly but begins again in obese individuals and pregnant women. This suggests that the pathway remains intact and could be manipulated to increase functional β-cell mass as a possible treatment for diabetic patients. NeuroD, a transcription factor within this pathway, is known to be critical for insulin gene expression in vitro. We present how NeuroD independently affects functional β-cell mass in terms of proliferation, secretion, and survival.