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miR-184 Regulates Pancreatic beta-Cell Function According to Glucose Metabolism
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Number of Authors: 18
2015 (English)In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 290, no 33, 20284-20294 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2015. Vol. 290, no 33, 20284-20294 p.
National Category
Biological Sciences
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URN: urn:nbn:se:su:diva-120680DOI: 10.1074/jbc.M115.658625ISI: 000359608900028OAI: oai:DiVA.org:su-120680DiVA: diva2:855933
Available from: 2015-09-22 Created: 2015-09-15 Last updated: 2017-12-01Bibliographically approved

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Friedländer, Marc R.
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Department of Molecular Biosciences, The Wenner-Gren InstituteScience for Life Laboratory (SciLifeLab)
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