| First Author | Tattikota SG | Year | 2015 |
| Journal | J Biol Chem | Volume | 290 |
| Issue | 33 | Pages | 20284-94 |
| PubMed ID | 26152724 | Mgi Jnum | J:317593 |
| Mgi Id | MGI:6844071 | Doi | 10.1074/jbc.M115.658625 |
| Citation | Tattikota SG, et al. (2015) miR-184 Regulates Pancreatic beta-Cell Function According to Glucose Metabolism. J Biol Chem 290(33):20284-94 |
| abstractText | In response to fasting or hyperglycemia, the pancreatic beta-cell alters its output of secreted insulin; however, the pathways governing this adaptive response are not entirely established. Although the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the beta-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the beta-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon the administration of a sucrose-rich diet in Drosophila, demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Argonaute2 in the presence of miR-184 rescued suppression of miR-375-targeted genes, suggesting these genes act in a coordinated manner during changes in the metabolic context. Together, these results highlight the adaptive role of miR-184 according to glucose metabolism and suggest the regulatory role of this miRNA in energy homeostasis is highly conserved. |
