Evidence map›Paper›PMID 27221121›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

MiR-206 is expressed in pancreatic islets and regulates glucokinase activity.

Manjula Vinod, Jay V Patankar, Vinay Sachdev, Saša Frank, Wolfgang F Graier, Dagmar Kratky, Gerhard M Kostner

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
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  8. Article
  9. Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022
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  11. Review
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  14. Review
  15. Article
  16. Glycogen Synthase Kinase 3 Beta Controls Presenilin-1-Mediated Endoplasmic Reticulum Ca²⁺ Leak Directed to Mitochondria in Pancreatic Islets and β-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019
    Article
  17. Article
  18. MicroRNA profiling of diabetic atherosclerosis in a rat model.European journal of medical research · 2018
    Article
  19. The Destiny of Glucose from a MicroRNA Perspective.Frontiers in endocrinology · 2018
    Review
  20. Review
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

7 authors at 1 institution in 1 country.

Manjula Vinod *Institute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Jay V Patankar *Institute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Vinay SachdevInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Saša FrankInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Wolfgang F GraierInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Dagmar KratkyInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Gerhard M KostnerInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Medical University of Graz · AT

Funding

Austrian Science Fund FWF F 3004Austrian Science Fund FWF P 27070Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

Glucose homeostasis is a complex indispensable process, and its dysregulation causes hyperglycemia and type 2 diabetes mellitus. Glucokinase (GK) takes a central role in these pathways and is thus rate limiting for glucose-stimulated insulin secretion (GSIS) from pancreatic islets. Several reports have described the transcriptional regulation of Gck mRNA, whereas its posttranscriptional mechanisms of regulation, especially those involving microRNAs (miR), are poorly understood. In this study, we investigated the role of miR-206 as a posttranscriptional regulator of Gck In addition, we examined the effects of miR-206 on glucose tolerance, GSIS, and gene expression in control and germ line miR-206 knockout (KO) mice fed either with chow or high-fat diet (HFD). MiR-206 was found in Gck-expressing tissues and was differentially altered in response to HFD feeding. Pancreatic islets showed the most profound induction in the expression of miR-206 in response to HFD. Chow- and HFD-fed miR-206KO mice have improved glucose tolerance and GSIS but unaltered insulin sensitivity. In silico analysis of Gck mRNA revealed a conserved 8-mer miR-206 binding site. Hence, the predicted regulation of Gck by miR-206 was confirmed in reporter and GK activity assays. Concomitant with increased GK activity, miR-206KO mice had elevated liver glycogen content and plasma lactate concentrations. Our findings revealed a novel mechanism of posttranscriptional regulation of Gck by miR-206 and underline the crucial role of pancreatic islet miR-206 in the regulation of whole body glucose homeostasis in a murine model that mimics the metabolic syndrome.

Indexed as

AnimalsComputer SimulationDiet, High-FatGlucokinaseGlucoseGlucose Tolerance TestGlycogenInsulinInsulin SecretionIslets of LangerhansLactic AcidLiverMaleMetabolic SyndromeMiceMice, KnockoutGlucokinaseGlucoseGlycogenInsulinLactic AcidMicroRNAsMirn206 microRNA, mouseRNA, Messengerglucose sensingglucose toleranceinsulin sensitivitymiR-206pancreatic islets

Identifiers

PMID27221121
PMCPMC4941929
OpenAlexW2395168079

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.