Evidence map›Paper›PMID 23668414›Full record

ArticleDiabetology & metabolic syndrome2013

The polygenetically inherited metabolic syndrome of male WOKW rats is associated with enhanced autophagy in adipose tissue.

Joanna Kosacka, Karoline Koch, Martin Gericke, Marcin Nowicki, John T Heiker, Ingrid Klöting, Michael Stumvoll, Matthias Blüher, Nora Klöting

Open access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
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  5. Article
  6. Adipocyte dysfunction, inflammation and metabolic syndrome.Reviews in endocrine & metabolic disorders · 2014
    Review
  7. Molecular regulation of autophagy and its implications for metabolic diseases.Current opinion in clinical nutrition and metabolic care · 2014
    Review
  8. Cross-talk between apoptosis and autophagy in lung epithelial cell death.Journal of biochemical and pharmacological research · 2014
    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

9 authors at 3 institutions in 1 country.

Joanna Kosacka *Department of Medicine, Endocrinology and Diabetes, University Leipzig, Leipzig, Germany.
Karoline Koch *IFB AdiposityDiseases, Junior Research Group 2 "Animal models of obesity", University Leipzig, Leipzig, Germany.
Martin GerickeInstitute of Anatomy, University Leipzig, Leipzig, Germany.
Marcin NowickiInstitute of Anatomy, University Leipzig, Leipzig, Germany.
John T HeikerDepartment of Medicine, Endocrinology and Diabetes, University Leipzig, Leipzig, Germany.
Ingrid KlötingDepartment of Laboratory Animal Science, University of Greifswald, Greifswald, Germany.
Michael StumvollDepartment of Medicine, Endocrinology and Diabetes, University Leipzig, Leipzig, Germany.
Matthias BlüherDepartment of Medicine, Endocrinology and Diabetes, University Leipzig, Leipzig, Germany.
Nora KlötingIFB AdiposityDiseases, Junior Research Group 2 "Animal models of obesity", University Leipzig, Leipzig, Germany.
Leipzig University · DEIFB Adiposity Diseases · DEUniversität Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies revealed that autophagy is up-regulated in obese individuals, as evidenced by increased expression of autophagy related genes. As argued elsewhere, it is possible that initially insulin resistance functions as an adaptive mechanism to increase autophagy in order to protect cells against death. We have shown that Wistar Ottawa Karlsburg W (RT1(u)) rats (WOKW) develop a metabolic syndrome with insulin resistance in adipose tissue, closely resembling the human disease. Therefore, the aim of this study was to characterize the autophagy phenotype in WOKW rats to clarify the interrelation between insulin resistance and autophagy in adipose tissue.

methodsSubcutaneous and epidydimal adipose tissue samples of 5-months-old WOKW and healthy LEW.1 W male rats were investigated and protein levels (Western blot and immunhistochemistry) of key autophagy genes, including Atg5, Atg7, LC3-II/LC3-I and apoptosis marker cleaved caspase-3 were analyzed.

resultsWOKW rats displayed a significant increase of autophagy related proteins (Atg5, Atg7) in adipose tissue compared with LEW.1 W. This increase was predominantly found in epididymal adipose tissue. Furthermore, the LC3-II/LC3-I ratio as a marker of autophagosomes was significantly up-regulated in subcutaneous adipose tissue of WOKW rats. Cleaved caspase-3 was just slightly detectable in visceral adipose tissue and not detected in subcutaneous fat.

conclusionInsulin resistance in adipose tissue of obese WOKW rats is associated with up-regulation of differing autophagy markers in visceral and subcutaneous fat depots. This fact not only qualifies the WOKW rat for further detailed analysis of genetic determinants of metabolic syndrome but also highlights its suitability for autophagy research.

Indexed as

Adipose tissueAtg5Atg7AutophagyInsulin resistanceWOKW

Identifiers

PMID23668414
PMCPMC3685536
OpenAlexW2115261650

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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.