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Journal of Undergraduate Research

Keywords

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

College

Life Sciences

Department

Nutrition, Dietetics, and Food Science

Abstract

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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