| First Author | Mandelbaum AD | Year | 2012 |
| Journal | Exp Diabetes Res | Volume | 2012 |
| Pages | 470302 | PubMed ID | 22991506 |
| Mgi Jnum | J:198397 | Mgi Id | MGI:5496503 |
| Doi | 10.1155/2012/470302 | Citation | Mandelbaum AD, et al. (2012) Dysregulation of Dicer1 in beta cells impairs islet architecture and glucose metabolism. Exp Diabetes Res 2012:470302 |
| abstractText | 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. |
