Evidence map›Paper›PMID 27496100›Full record

ArticleCardiovascular diabetology2016

Transcriptomic alterations in the heart of non-obese type 2 diabetic Goto-Kakizaki rats.

Márta Sárközy, Gergő Szűcs, Veronika Fekete, Márton Pipicz, Katalin Éder, Renáta Gáspár, Andrea Sója, Judit Pipis, Péter Ferdinandy, Csaba Csonka and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  8. A new hyperpolarizedScientific reports · 2019
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  12. An Update on the Multifaceted Roles of STAT3 in the Heart.Frontiers in cardiovascular medicine · 2019
    Review
  13. Article
  14. Effects of Cardiovascular Risk Factors on Cardiac STAT3.International journal of molecular sciences · 2018
    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

11 authors at 2 institutions in 1 country.

Márta SárközyDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Gergő SzűcsDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Veronika FeketeDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Márton PipiczDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Katalin ÉderDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Renáta GáspárDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Andrea SójaDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Judit PipisPharmahungary Group, Szeged, Hungary.
Péter FerdinandyPharmahungary Group, Szeged, Hungary.
Csaba CsonkaDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Tamás CsontDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary. csont.tamas@med.u-szeged.hu.
University of Szeged · HUSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is a spectacular rise in the global prevalence of type 2 diabetes mellitus (T2DM) due to the worldwide obesity epidemic. However, a significant proportion of T2DM patients are non-obese and they also have an increased risk of cardiovascular diseases. As the Goto-Kakizaki (GK) rat is a well-known model of non-obese T2DM, the goal of this study was to investigate the effect of non-obese T2DM on cardiac alterations of the transcriptome in GK rats.

methodsFasting blood glucose, serum insulin and cholesterol levels were measured at 7, 11, and 15 weeks of age in male GK and control rats. Oral glucose tolerance test and pancreatic insulin level measurements were performed at 11 weeks of age. At week 15, total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 41,012 genes, and then expression of selected genes was confirmed by qRT-PCR. Gene ontology and protein-protein network analyses were performed to demonstrate potentially characteristic gene alterations and key genes in non-obese T2DM.

resultsFasting blood glucose, serum insulin and cholesterol levels were significantly increased, glucose tolerance and insulin sensitivity were significantly impaired in GK rats as compared to controls. In hearts of GK rats, 204 genes showed significant up-regulation and 303 genes showed down-regulation as compared to controls according to microarray analysis. Genes with significantly altered expression in the heart due to non-obese T2DM includes functional clusters of metabolism (e.g. Cyp2e1, Akr1b10), signal transduction (e.g. Dpp4, Stat3), receptors and ion channels (e.g. Sln, Chrng), membrane and structural proteins (e.g. Tnni1, Mylk2, Col8a1, Adam33), cell growth and differentiation (e.g. Gpc3, Jund), immune response (e.g. C3, C4a), and others (e.g. Lrp8, Msln, Klkc1, Epn3). Gene ontology analysis revealed several significantly enriched functional inter-relationships between genes influenced by non-obese T2DM. Protein-protein interaction analysis demonstrated that Stat is a potential key gene influenced by non-obese T2DM.

conclusionsNon-obese T2DM alters cardiac gene expression profile. The altered genes may be involved in the development of cardiac pathologies and could be potential therapeutic targets in non-obese T2DM.

Indexed as

TranscriptomeAnimalsBlood GlucoseDiabetes Mellitus, Type 2Gene ExpressionGene Expression RegulationHeartMaleMesothelinMetabolic SyndromeMyocardiumRatsTranscription, GeneticBlood GlucoseMesothelinMsln protein, ratDNA microarrayGOInherited diabetes mellitusInsulin resistanceMyocardiumNon-obese type 2 diabetes mellitusSpontaneous diabetes mellitusString

Identifiers

PMID27496100
PMCPMC4975916
OpenAlexW2489317406

What OpenQuestion holds

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LicenceCC BY
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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.