Jensen, Daelin; Aitken, Talon; Baxter, Melanie (Brigham Young University)
Faculty Advisor: Tessem, Jeffery (Brigham Young University; Nutrition, Dietetics, and Food Science)
As of 2017, over 400 million people were diagnosed with diabetes mellitus. This is becoming a worldwide concern as the number of people affected by diabetes is growing at an alarming rate. Functional pancreatic β-cell mass is responsible for maintaining healthy blood glucose levels through the production of insulin. A hallmark of both type 1 and type 2 diabetes is a relative or absolute loss of functional β-cell mass and, consequently, decreased insulin production. Two possible approaches for replenishing the β-cells are: 1) replacement through cadaveric donors and 2) regeneration of endogenous β-cells. A major impediment to these approaches is that aged β-cells are refractory to genes that are known to induce proliferation in young β-cells. It is currently unknown why aged β-cells are refractory. . We hypothesized that age-dependent changes to the proliferative capacity of β-cells are influenced by increasing levels of cyclin-dependent kinase inhibitors (CDKI). CDKI's bind to cyclin-dependent kinases, effectively halting the cell cycle and proliferation. Here, we demonstrate the expression of the Ink4 and Cip/Kip families of CDKI's by mRNA and protein expression in five week old and five month old Wistar rat β-cells. Greater understanding of the proliferative mechanisms of the β-cell will allow greater application of the aforementioned treatments.