Evidence map›Paper›PMID 26474776›Full record

ArticleDiabetologia2016

Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets.

Ksenia Tugay, Claudiane Guay, Ana C Marques, Florent Allagnat, Jonathan M Locke, Lorna W Harries, Guy A Rutter, Romano Regazzi

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Frontiers in endocrinology · 2025
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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

8 authors at 3 institutions in 2 countries.

Ksenia TugayDepartment of Fundamental Neurosciences, University of Lausanne, Rue du Bugnon 9, CH-1005, Lausanne, Switzerland.
Claudiane GuayDepartment of Fundamental Neurosciences, University of Lausanne, Rue du Bugnon 9, CH-1005, Lausanne, Switzerland.
Ana C MarquesDepartment of Physiology, University of Lausanne, Lausanne, Switzerland.
Florent AllagnatDepartment of Physiology, University of Lausanne, Lausanne, Switzerland.
Jonathan M LockeInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK.
Lorna W HarriesInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK.
Guy A RutterSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK.
Romano RegazziDepartment of Fundamental Neurosciences, University of Lausanne, Rue du Bugnon 9, CH-1005, Lausanne, Switzerland. romano.regazzi@unil.ch.
University of Lausanne · CHUniversity of Exeter · GBImperial College London · GB

Funding

Medical Research Council MR/J0003042/1Medical Research Council MR/K001981/1Wellcome Trust 089845/Z/09/ZWellcome Trust 098424Wellcome Trust WT098424AIA
6 · The paper itself

Abstract

aims/hypothesisAgeing can lead to reduced insulin sensitivity and loss of pancreatic beta cell function, predisposing individuals to the development of diabetes. The aim of this study was to assess the contribution of microRNAs (miRNAs) to age-associated beta cell dysfunction.

methodsThe global mRNA and miRNA profiles of 3- and 12-month-old rat islets were collected by microarray. The functional impact of age-associated differences in miRNA expression was investigated by mimicking the observed changes in primary beta cells from young animals.

resultsBeta cells from 12-month-old rats retained normal insulin content and secretion, but failed to proliferate in response to mitotic stimuli. The islets of these animals displayed modifications at the level of several miRNAs, including upregulation of miR-34a, miR-124a and miR-383, and downregulation of miR-130b and miR-181a. Computational analysis of the transcriptomic modifications observed in the islets of 12-month-old rats revealed that the differentially expressed genes were enriched for miR-34a and miR-181a targets. Indeed, the induction of miR-34a and reduction of miR-181a in the islets of young animals mimicked the impaired beta cell proliferation observed in old animals. mRNA coding for alpha-type platelet-derived growth factor receptor, which is critical for compensatory beta cell mass expansion, is directly inhibited by miR34a and is likely to be at least partly responsible for the effects of this miRNA. CONCLUSIONS/

interpretationChanges in the level of specific miRNAs that occur during ageing affect the proliferative capacity of beta cells. This might reduce their ability to expand under conditions of increased insulin demand, favouring the development of type 2 diabetes.

Indexed as

AgingGene Expression RegulationAnimalsApoptosisCell ProliferationDiabetes Mellitus, Type 2Disease Models, AnimalHumansInsulinInsulin ResistanceInsulin-Secreting CellsIslets of LangerhansMaleMicroRNAsRatsRats, WistarInsulinMicroRNAsMIRN124 microRNA, ratMIRN130 microRNA, ratMIRN181 microRNA, ratMIRN34 microRNA, ratMIRN383 microRNA, ratRNA, Messenger

Identifiers

PMID26474776
PMCPMC4670458
OpenAlexW1940684812

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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.