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Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.
MiR-184 regulates pancreatic β-cell function according to glucose metabolism.
J. Biol. Chem. 290, 20284-20294 (2015)
In response to fasting or hyperglycemia, the pancreatic β-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While 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 β-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 β-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon administration of a sucrose-rich diet in Drosophila demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 (Ago2) remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Ago2 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.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Argonaute ; Beta Cell (b-cell) ; Glucose Metabolism ; Insulin ; Insulin Secretion ; Microrna (mirna) ; Microrna Mechanism ; Pancreatic Islet; Insulin-secretion; In-vivo; Drosophila; Protein; Stress; Replication; Micrornas; Reveals; Differentiation; Proliferation
ISSN (print) / ISBN
0021-9258
e-ISSN
1083-351X
Zeitschrift
Journal of Biological Chemistry, The
Quellenangaben
Band: 290,
Heft: 33,
Seiten: 20284-20294
Verlag
American Society for Biochemistry and Molecular Biology
Verlagsort
Bethesda
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Obesity (IDO)