Journal of Undergraduate Research


Nr4a1, B-cell glucose, insulin secretion, cellular survival


Life Sciences


Nutrition, Dietetics, and Food Science


In 2010, diabetes was the 7th leading cause of death in America, and as of 2014, 9% of the world’s adult population was affected by it. In both Type I (T1D) and Type II diabetes (T2D), a loss of β-cell mass and overall function is observed. β-cells essentially stop proliferating after adolescence, therefore developing mechanisms to increase function and/or induce proliferation in β-cells could serve as a powerful treatment and even a cure for both T1D and T2D. Overexpression of the β-cell transcription factor Nkx6.1 induces β-cell proliferation (1) and up-regulates expression of the nuclear receptor Nr4a1 (2). Nr4a1 has been shown to be necessary and sufficient for Nkx6.1-mediated β-cell proliferation (2). In addition to its proliferative effects, we also know that Nkx6.1 is necessary for maintaining proper β-cell function (3). To further investigate the mechanisms of β-cell proliferation and maintenance, we bred mice that lacked the Nr4a1 gene, anticipating that these animals would exhibit increased blood glucose levels under normal conditions, as well as during a glucose tolerance test. We also examined relative immunity cell levels in the knockout animals.

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