Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
Diabetes currently affects over 30 million Americans and 422 million people worldwide. Additionally, over 80 million Americans are classified as pre-diabetic. Normally, insulin-secreting β-cells in the pancreas regulate proper glucose absorption and storage. Type 1 (T1D) and Type 2 (T2D) diabetes are characterized by decreased functional β-cell mass and insulin production. Pancreatic, insulin-secreting β-cells are either lost in T1D, or the body’s insulin-sensitive cells become insulin resistant in T2D. β-cells stop proliferating soon after birth, except for a few occasions such as extreme obesity or pregnancy. Consequently, we believe that there are key gene(s) that, when activated, lead to β-cell proliferation. Finding which gene(s) lead to proliferation will allow us to develop and define strategies for replacement of functional β-cells to cure both forms of diabetes. The gene Nkx2.2 is vital to the differentiation and specification of the β-cell, but its specific effect on β-cell function is still unclear. In order to better understand the independent role of Nkx2.2 on β-cell function, we show the effect of Nkx2.2 overexpression on β-cell proliferation, survival, and insulin secretion.