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MiR-184 regulates pancreatic β-cell function according to glucose metabolism.

Tattikota, Sudhir G ; Rathjen, Thomas ; Hausser, Jean ; Khedkar, Aditya ; Kabra, Uma D ; Pandey, Varun K ; Sury, Matthias ; Wessels, Hans-Hermann ; Mollet, Ines LU and Eliasson, Lena LU orcid , et al. (2015) In Journal of Biological Chemistry 290(33). p.20284-20294
Abstract
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Biological Chemistry
volume
290
issue
33
pages
20284 - 20294
publisher
American Society for Biochemistry and Molecular Biology
external identifiers
  • pmid:26152724
  • wos:000359608900028
  • scopus:84939825167
  • pmid:26152724
ISSN
1083-351X
DOI
10.1074/jbc.M115.658625
language
English
LU publication?
yes
id
2b90dd2a-4af7-4152-83c5-cf5812fba127 (old id 7750172)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26152724?dopt=Abstract
date added to LUP
2016-04-01 09:57:28
date last changed
2022-01-25 18:21:09
@article{2b90dd2a-4af7-4152-83c5-cf5812fba127,
  abstract     = {{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.}},
  author       = {{Tattikota, Sudhir G and Rathjen, Thomas and Hausser, Jean and Khedkar, Aditya and Kabra, Uma D and Pandey, Varun K and Sury, Matthias and Wessels, Hans-Hermann and Mollet, Ines and Eliasson, Lena and Selbach, Matthias and Zinzen, Robert P and Zavolan, Mihaela and Kadener, Sebastian and Tschöp, Matthias and Jastroch, Martin and Friedländer, Marc R and Poy, Matthew N}},
  issn         = {{1083-351X}},
  language     = {{eng}},
  number       = {{33}},
  pages        = {{20284--20294}},
  publisher    = {{American Society for Biochemistry and Molecular Biology}},
  series       = {{Journal of Biological Chemistry}},
  title        = {{MiR-184 regulates pancreatic β-cell function according to glucose metabolism.}},
  url          = {{https://lup.lub.lu.se/search/files/1423754/8867381._Chem_mollet_et_al}},
  doi          = {{10.1074/jbc.M115.658625}},
  volume       = {{290}},
  year         = {{2015}},
}