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Experimental Diabetes Research
Volume 2012 (2012), Article ID 470302, 8 pages
Research Article

Dysregulation of Dicer1 in Beta Cells Impairs Islet Architecture and Glucose Metabolism

1Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel
2Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel

Received 12 January 2012; Revised 3 May 2012; Accepted 17 May 2012

Academic Editor: Anandwardhan Hardikar

Copyright © 2012 Amitai D. Mandelbaum 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.


microRNAs (miRNAs) play important roles in pancreas development and in regulation of insulin expression in the adult. Here we show that loss of miRNAs activity in beta-cells during embryonic development results in lower beta-cell mass and in impaired glucose tolerance. Dicer1-null cells initially constitute a significant portion of the total beta-cell population. However, during postnatal development, Dicer1-null cells are depleted. Furthermore, wild-type beta cells are repopulating the islets in complex compensatory dynamics. Because loss of Dicer1 is also associated with changes in the distribution of membranous E-cadherin, we hypothesized that E-cadherin activity may play a role in beta cell survival or islet architecture. However, genetic loss of E-cadherin function does not impair islet architecture, suggesting that miRNAs likely function through other or redundant effectors in the endocrine pancreas.