Evidence map›Paper›PMID 34149616›Full record

ArticleFrontiers in endocrinology2021

Metformin Improves Autonomic Nervous System Imbalance and Metabolic Dysfunction in Monosodium L-Glutamate-Treated Rats.

Claudinéia Conationi da Silva Franco, Carina Previate, Amanda Bianchi Trombini, Rosiane Aparecida Miranda, Luiz Felipe Barella, Lucas Paulo Jacinto Saavedra, Júlio Cezar de Oliveira, Kelly Valério Prates, Laize Peron Tófolo, Tatiane Aparecida Ribeiro and 13 more

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In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  4. Review
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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

23 authors at 5 institutions in 1 country.

Claudinéia Conationi da Silva FrancoLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Carina PreviateLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Amanda Bianchi TrombiniLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Rosiane Aparecida MirandaCarlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Luiz Felipe BarellaLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Lucas Paulo Jacinto SaavedraLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Júlio Cezar de OliveiraInstitute of Health Sciences, Federal University of Mato Grosso-Sinop, Sinop, Brazil.
Kelly Valério PratesLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Laize Peron TófoloLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Tatiane Aparecida RibeiroLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Audrei PavanelloLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Ananda MaltaLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Isabela Peixoto MartinsLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Veridiana Motta MoreiraLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Camila Cristina Ianoni MatiussoLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Flávio Andrade FranciscoLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Vander Silva AlvesLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Ana Maria Praxedes de MoraesLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Juliane Rocha de Sant AnnaLaboratory of Mutagenesis & Genetics, Department of Cell Biology and Genetics, State University of Maringá, Maringá, Brazil.
Marialba Avezum Alves de Castro PradoLaboratory of Mutagenesis & Genetics, Department of Cell Biology and Genetics, State University of Maringá, Maringá, Brazil.
Rodrigo Mello GomesDepartment of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil.
Elaine VieiraPostgraduate Program on Physical Education, University Católica of Brasília, Brasília, Brazil.
Paulo Cezar de Freitas MathiasLaboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Brazil.
Universidade Estadual de Maringá · BRUniversidade Católica de Brasília · BRUniversidade Federal de Goiás · BRUniversidade Federal de Mato Grosso · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metformin is an antidiabetic drug used for the treatment of diabetes and metabolic diseases. Imbalance in the autonomic nervous system (ANS) is associated with metabolic diseases. This study aimed to test whether metformin could improve ANS function in obese rats. Obesity was induced by neonatal treatment with monosodium L-glutamate (MSG). During 21-100 days of age, MSG-rats were treated with metformin 250 mg/kg body weight/day or saline solution. Rats were euthanized to evaluate biometric and biochemical parameters. ANS electrical activity was recorded and analyzed. Metformin normalized the hypervagal response in MSG-rats. Glucose-stimulated insulin secretion in isolated pancreatic islets increased in MSG-rats, while the cholinergic response decreased. Metformin treatment normalized the cholinergic response, which involved mostly the M3 muscarinic acetylcholine receptor (M3 mAChR) in pancreatic beta-cells. Protein expression of M3 mAChRs increased in MSG-obesity rats, while metformin treatment decreased the protein expression by 25%. In conclusion, chronic metformin treatment was effective in normalizing ANS activity and alleviating obesity in MSG-rats.

Indexed as

AcetylcholineAnimalsAutonomic Nervous SystemGlucoseHypoglycemic AgentsInsulin-Secreting CellsMaleMetforminNeostigmineObesityRatsRats, WistarReceptor, Muscarinic M3Sodium GlutamateVagus NerveAcetylcholineGlucoseHypoglycemic AgentsMetforminNeostigmineReceptor, Muscarinic M3Sodium Glutamateacetylcholineautonomic nervous systeminsulin secretionmetforminMSG-obese rats

Identifiers

PMID34149616
PMCPMC8212417
OpenAlexW3172891882

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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.