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2018 Abstracts

Cyclin Dependent Kinase Inhibitors Play a Role in Blocking β cell Proliferation

Parker Booren; Talon Aitken; Samuel Grover; Nathan Jensen; Jackie Crabtree, Brigham Young University

The number of people affected by diabetes is continually rising, affecting over 400 million people worldwide as of today. The pancreas contains β cells, which secrete insulin, leading to proper glucose absorption and storage. Both Type 1 and Type 2 diabetes are characterized by decreased functional β cell mass and, consequently, decreased insulin production. Increasing the amount of functional β cells will lead to increased insulin production and better management or a possible treatment strategy for the disease. β cells cease to proliferate in humans at a young age, and rats follow a similar model. We aimed to determine why aged β cells do not replicate, and turned to the cell cycle to determine this. The cell cycle is tightly regulated by cyclin-dependent kinases. Cells also produce proteins known as cyclin-dependent kinase inhibitors(CDKI’s), which bind to cyclin dependent kinases, effectively shutting down cell proliferation. We seek to examine the location and roles of CDKI’s in the cell cycle to determine the role they play in inhibiting β cell proliferation. Several CDKI’s, namely Ink4a -Ink4d, Cip1 and Kip1, were examined to determine the role they play in rat β cells. These results represent a significant step to identifying the mechanism of β cell proliferation, and ultimately leading to investigations that would increase β cell mass, insulin secretion, and glucose homeostasis.