Dysregulation of Dicer1 in Beta Cells Impairs Islet Architecture and Glucose Metabolism. (6th September 2012)

• Record Type: Journal Article
• Authors: Mandelbaum, Amitai D.; Melkman-Zehavi, Tal; Oren, Roni; Kredo-Russo, Sharon; Nir, Tomer; Dor, Yuval; Hornstein, Eran
• Other Names: Hardikar Anandwardhan Academic Editor.
• Is Part Of: Experimental diabetes research. Volume 2012(2012)
• Publication Date: 2012-09-06
• Subjects: Diabetes -- Research -- Periodicals; Diabetes -- Research; Periodicals; 616.462
• DOI: 10.1155/2012/470302
• Languages: English
• ISSNs: 1687-5214

Abstract

Abstract : 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.