Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 348, Issue 1, Pages 297-304Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2011.09.013
Keywords
beta-cell apoptosis; Cidea; FFA; FoxO1
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Chronic exposure to free fatty acid (FFA) induces pancreatic beta-cell apoptosis, which may contribute to the development of type 2 diabetes. The cell death-inducing DNA fragmentation factor alpha-like effector (CIDE) family is involved in type 2 diabetes with obesity. In the present study, we found that only apoptosis-inducing FFA upregulated Cidea, and both apoptosis and Cidea were upregulated most strongly by palmitic acid, suggesting that the expression of Cidea is positively correlated with apoptosis. In contrast, there were weak correlations between Cideb and Cidec expression, and apoptosis. Furthermore, suppression of Cidea inhibited palmitic acid-induced apoptosis. Finally, suppression of FoxO1 inhibited palmitic acid-induced Cidea upregulation and apoptosis. These results indicate that Cidea is a critical regulator of FFA-induced apoptosis as a novel downstream target for FoxO1 in beta-cells, suggesting that suppression of Cidea is a potentially useful therapeutic approach for protecting against beta-cell loss in type 2 diabetes. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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