Evidence map›Paper›PMID 33300293›Full record

ArticleJournal of cellular and molecular medicine2021

The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure.

Paula Schmidt Azevedo, Bertha F Polegato, Sergio Paiva, Nara Costa, Priscila Santos, Silmeia Bazan, Ana Angelica Henrique Fernandes, Alexandre Fabro, Vanessa Pires, Suzana E Tanni and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

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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

17 authors at 4 institutions in 1 country.

Paula Schmidt AzevedoDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.ORCID 0000-0002-5843-6232
Bertha F PolegatoDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.ORCID 0000-0002-2875-9532
Sergio PaivaDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Nara CostaFaculty of Nutrition, UFG - Univ Federal de Goiás, Goiânia, Brazil.
Priscila SantosDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Silmeia BazanDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Ana Angelica Henrique FernandesDepartment of Chemical and Biological Sciences, São Paulo State University-UNESP, Botucatu, Brazil.
Alexandre FabroDepartment of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Vanessa PiresDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Suzana E TanniDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Filipe Leal PereiraDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Angelo LoDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Leticia GrassiDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Dijon CamposDepartment of Pathology and Legal Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Vickeline AndrocioliExperimental Research Unit - UNIPEX, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Leonardo ZornoffDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Marcos MinicucciDepartment of Internal Medicine, Botucatu Medical School, São Paulo State University-UNESP, Botucatu, Brazil.
Universidade Estadual Paulista (Unesp) · BRUniversidade de São Paulo · BRCentro Universitário de João Pessoa · BRUniversidade Federal de Goiás · BR

Funding

Conselho Nacional de Pesquisa, Ministério da Ciência, Tecnologia, Inovações e ComunicaçõesCoordenação de Aperfeiçoamento de Pessoal de Nível Superior 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/24197-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/14547-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/25676-5
6 · The paper itself

Abstract

The aim of this study is to evaluate whether the alterations in glucose metabolism and insulin resistance are mechanisms presented in cardiac remodelling induced by the toxicity of cigarette smoke. Male Wistar rats were assigned to the control group (C; n = 12) and the cigarette smoke-exposed group (exposed to cigarette smoke over 2 months) (CS; n = 12). Transthoracic echocardiography, blood pressure assessment, serum biochemical analyses for catecholamines and cotinine, energy metabolism enzymes activities assay; HOMA index (homeostatic model assessment); immunohistochemistry; and Western blot for proteins involved in energy metabolism were performed. The CS group presented concentric hypertrophy, systolic and diastolic dysfunction, and higher oxidative stress. It was observed changes in energy metabolism, characterized by a higher HOMA index, lower concentration of GLUT4 (glucose transporter 4) and lower 3-hydroxyl-CoA dehydrogenase activity, suggesting the presence of insulin resistance. Yet, the cardiac glycogen was depleted, phosphofructokinase (PFK) and lactate dehydrogenase (LDH) increased, with normal pyruvate dehydrogenase (PDH) activity. The activity of citrate synthase, mitochondrial complexes and ATP synthase (adenosine triphosphate synthase) decreased and the expression of Sirtuin 1 (SIRT1) increased. In conclusion, exposure to cigarette smoke induces cardiac remodelling and dysfunction. The mitochondrial dysfunction and heart damage induced by cigarette smoke exposure are associated with insulin resistance and glucose metabolism changes.

Indexed as

Insulin ResistanceVentricular RemodelingAnimalsCatecholaminesCotinineElectrocardiographyEnergy MetabolismGlucoseMaleOxidative StressRatsRats, WistarSmokingCatecholaminesCotinineGlucosecardiac remodellingcigarette smokeglucose metabolismheart failureventricular remodelling

Identifiers

PMID33300293
PMCPMC7812248
OpenAlexW3110740319

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.