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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 9648769, 9 pages
Research Article

Nr2e1 Deficiency Augments Palmitate-Induced Oxidative Stress in Beta Cells

Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China

Received 13 April 2015; Revised 12 July 2015; Accepted 15 July 2015

Academic Editor: Ada Popolo

Copyright © 2016 Xiaoli Shi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nuclear receptor subfamily 2 group E member 1 (Nr2e1) has been regarded as an essential regulator of the growth of neural stem cells. However, its function elsewhere is unknown. In the present study, we generated Nr2e1 knockdown MIN6 cells and studied whether Nr2e1 knockdown affected basal beta cell functions such as proliferation, cell death, and insulin secretion. We showed that knockdown of Nr2e1 in MIN6 cells resulted in increased sensitivity to lipotoxicity, decreased proliferation, a partial G0/G1 cell-cycle arrest, and higher rates of apoptosis. Moreover, Nr2e1 deficiency exaggerates palmitate-induced impairment in insulin secretion. At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress. Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2. Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.