Dysregulation of Dicer1 in beta cells impairs islet architecture and glucose metabolism

Amitai D. Mandelbaum, Tal Melkman-Zehavi, Roni Oren, Sharon Kredo-Russo, Tomer Nir, Yuval Dor, Eran Hornstein*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


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.

Original languageAmerican English
Article number470302
JournalExperimental Diabetes Research
StatePublished - 2012


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