Evidence map›Paper›PMID 30154842›Full record

ArticleInternational journal of endocrinology2018

Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects.

Edna Berzabá-Evoli, Cecilia Zazueta, Jarumi Hishel Cruz Hernández, Nancy Patricia Gómez-Crisóstomo, Isela Esther Juárez-Rojop, Erick Natividad De la Cruz-Hernández, Eduardo Martínez-Abundis

Open access · goldAbstract read
In one paragraph

Article in International journal of endocrinology, 2018. 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
0.8field-weighted citation impact, top 27% 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, 10 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    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

7 authors at 2 institutions in 1 country.

Edna Berzabá-EvoliLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.
Cecilia ZazuetaDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología (I. Ch.), 14080 Tlalpan, MEX, Mexico.ORCID 0000-0003-1068-316X
Jarumi Hishel Cruz HernándezLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.
Nancy Patricia Gómez-CrisóstomoLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.ORCID 0000-0001-9258-7125
Isela Esther Juárez-RojopResearch Center, Academic Division of Health Sciences (DACS), Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.
Erick Natividad De la Cruz-HernándezLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.
Eduardo Martínez-AbundisLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, Mexico.ORCID 0000-0001-6369-5880
Universidad Juárez Autónoma de Tabasco · MXInstituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFunctional receptors for leptin were described on the surface of cardiomyocytes, and there was a prohypertrophic effect with high concentrations of the cytokine. Therefore, leptin could be a link between obesity and the prevalence of cardiovascular diseases. On the other hand, a deleterious effect of leptin on mitochondrial performance was described, which was also associated with the evolution of cardiac hypertrophy to heart failure. The goal of our study was to analyze the effect of the exposure of rat hearts to a high concentration of leptin on cardiac and mitochondrial function.

methodsRat hearts were perfused continuously with or without 3.1 nM leptin for 1, 2, 3, or 4 hours. Homogenates and mitochondria were prepared by centrifugation and analyzed for cardiac actin, STAT3, and pSTAT3 by Western blotting, as well as for mitochondrial oxidative phosphorylation, membrane potential, swelling, calcium transport, and content of oxidized lipids.

resultsIn our results, leptin induced an increased rate-pressure product as a result of increased heart rate and contraction force, as well oxidative stress. In addition, mitochondrial dysfunction expressed as a loss of membrane potential, decreased ability for calcium transport and retention, faster swelling, and less respiratory control was observed.

conclusionsOur results support the role of leptin as a deleterious factor for cardiac function and indicates that mitochondrial dysfunction could be a trigger for cardiac hypertrophy and failure.

Identifiers

PMID30154842
PMCPMC6093050
OpenAlexW2887612281

What OpenQuestion holds

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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.