Evidence map›Paper›PMID 26152724›Full record

ArticleThe Journal of biological chemistry2015

miR-184 Regulates Pancreatic β-Cell Function According to Glucose Metabolism.

Sudhir G Tattikota, Thomas Rathjen, Jean Hausser, Aditya Khedkar, Uma D Kabra, Varun Pandey, Matthias Sury, Hans-Hermann Wessels, Inês G Mollet, Lena Eliasson and 8 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  8. Nutrient dependentmicroPublication biology · 2022
    Article
  9. Article
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  11. Review
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  14. The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Epigenetics in β-cell adaptation and type 2 diabetes.Current opinion in pharmacology · 2020
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 4 countries.

Sudhir G TattikotaFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Thomas RathjenFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Jean HausserComputational and Systems Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland.
Aditya KhedkarFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Uma D KabraInstitute for Diabetes and Obesity, Helmholtz Centre for Health and Environment and Division of Metabolic Diseases, Technical University Munich, 85748 Munich, Germany.
Varun PandeyBiological Chemistry Department, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.
Matthias SuryFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Hans-Hermann WesselsFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Inês G MolletIslet cell exocytosis, Lund University Diabetes Center, CRC 91-11, Jan Waldenströms gata 35, 20502 Malmö, Sweden, and.
Lena EliassonIslet cell exocytosis, Lund University Diabetes Center, CRC 91-11, Jan Waldenströms gata 35, 20502 Malmö, Sweden, and.
Matthias SelbachFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Robert P ZinzenFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany.
Mihaela ZavolanComputational and Systems Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland.
Sebastian KadenerBiological Chemistry Department, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.
Matthias H TschöpInstitute for Diabetes and Obesity, Helmholtz Centre for Health and Environment and Division of Metabolic Diseases, Technical University Munich, 85748 Munich, Germany.
Martin JastrochInstitute for Diabetes and Obesity, Helmholtz Centre for Health and Environment and Division of Metabolic Diseases, Technical University Munich, 85748 Munich, Germany.
Marc R FriedländerScience for Life Laboratory, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 17121 Stockholm, Sweden.
Matthew N PoyFrom the Max Delbrueck Center for Molecular Medicine, 13125 Berlin, Germany, matthew.poy@mdc-berlin.de.
Max Delbrück Center · DETechnical University of Munich · DEHebrew University of Jerusalem · ILUniversity of Basel · CHStockholm University · SE

Funding

European Research Council 260744
6 · The paper itself

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. 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 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 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.

Indexed as

AnimalsArgonaute ProteinsCell LineGlucoseHomeostasisIslets of LangerhansMiceMicroRNAsMitochondriaAgo2 protein, mouseArgonaute ProteinsGlucoseMicroRNAsMIRN184 microRNA, mouseArgonautebeta cell (B-cell)glucose metabolisminsulininsulin secretionmicroRNA mechanismmicroRNA (miRNA)pancreatic islet

Identifiers

PMID26152724
PMCPMC4536436
OpenAlexW1944402090

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.