Evidence map›Paper›PMID 30711402›Full record

ArticleMolecular metabolism2019

miR-132-3p is a positive regulator of alpha-cell mass and is downregulated in obese hyperglycemic mice.

Rodolphe Dusaulcy, Sandra Handgraaf, Florian Visentin, Christian Vesin, Jacques Philippe, Yvan Gosmain

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. miR-27a Regulates Sheep Adipocyte Differentiation by TargetingAnimals : an open access journal from MDPI · 2021
    Article
  5. Article
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  10. Article
  11. Review
  12. MiR-876-3p targets KIF20A to block JAK2/STAT3 pathway in glioma.American journal of translational research · 2019
    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

6 authors at 1 institution in 2 countries.

Rodolphe DusaulcyLaboratory of Molecular Diabetes, Division of Endocrinology, Diabetes, Hypertension and Nutrition, University Hospital/Diabetes Center/University of Geneva Medical School, Geneva, Switzerland. Electronic address: rodolphe.dusaulcy@unige.ch.
Sandra HandgraafLaboratory of Molecular Diabetes, Division of Endocrinology, Diabetes, Hypertension and Nutrition, University Hospital/Diabetes Center/University of Geneva Medical School, Geneva, Switzerland.
Florian VisentinLaboratory of Molecular Diabetes, Division of Endocrinology, Diabetes, Hypertension and Nutrition, University Hospital/Diabetes Center/University of Geneva Medical School, Geneva, Switzerland.
Christian VesinDepartment of Cell Physiology and Metabolism, University of Geneva School of Medicine, Geneva, Switzerland.
Jacques PhilippeLaboratory of Molecular Diabetes, Division of Endocrinology, Diabetes, Hypertension and Nutrition, University Hospital/Diabetes Center/University of Geneva Medical School, Geneva, Switzerland.
Yvan GosmainLaboratory of Molecular Diabetes, Division of Endocrinology, Diabetes, Hypertension and Nutrition, University Hospital/Diabetes Center/University of Geneva Medical School, Geneva, Switzerland.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveDiabetes is a complex disease implicating several organs and cell types. Within the islets, dysregulation occurs in both alpha- and beta-cells, leading to defects of insulin secretion and increased glucagon secretion. Dysregulation of alpha-cells is associated with transcriptome changes. We hypothesized that microRNAs (miRNAs) which are negative regulators of mRNA stability and translation could be involved in alpha-cell alterations or adaptations during type 2 diabetes.

methodsmiRNA microarray analyses were performed on pure alpha- and beta-cells from high-fat diet fed obese hyperglycemic mice and low-fat diet fed controls. Then, the most regulated miRNA was overexpressed or inhibited in primary culture of mouse and human alpha-cells to determine its molecular and functional impact.

results16 miRNAs were significantly regulated in alpha-cells of obese hyperglycemic mice and 28 in beta-cells. miR-132-3p had the strongest regulation level in alpha-cells, where it was downregulated, while we observed an opposite upregulation in beta-cells. In vitro experiments showed that miR-132-3p, which is inversely regulated by somatostatin and cAMP, is a positive modulator of alpha-cell proliferation and implicated in their resistance to apoptosis. These effects are associated with the regulation of a series of genes, including proliferation and stress markers Mki67 and Bbc3 in mouse and human alpha-cells, potentially involved in miR-132-3p functions.

conclusionsDownregulation of miR-132-3p in alpha-cells of obese diabetic mice may constitute a compensatory mechanism contributing to keep glucagon-producing cell number constant in diabetes.

Indexed as

Down-RegulationAnimalsCells, CulturedGlucagon-Secreting CellsHumansMiceMice, ObeseMicroRNAsObesityMicroRNAsMIRN132 microRNA, humanMIRN132 microRNA, mouseAlpha-cellApoptosisGlucagonmiR-132-3pProliferationType 2 diabetes

Identifiers

PMID30711402
PMCPMC6437597
OpenAlexW2909958263

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.