Evidence map›Paper›PMID 27538526›Full record

ArticleCardiovascular diabetology2016

Glucose intolerance after chronic stress is related with downregulated PPAR-γ in adipose tissue.

Vitor H Pereira, Fernanda Marques, Vânia Lages, Filipa G Pereira, Alexandre Patchev, Osborne F X Almeida, Joana Almeida-Palha, Nuno Sousa, João J Cerqueira

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition.Laboratory investigation; a journal of technical methods and pathology · 2018
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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

9 authors at 2 institutions in 2 countries.

Vitor H PereiraLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
Fernanda MarquesLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
Vânia LagesLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
Filipa G PereiraLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
Alexandre PatchevMax-Planck-Institute of Psychiatry, Munich, Germany.
Osborne F X AlmeidaMax-Planck-Institute of Psychiatry, Munich, Germany.
Joana Almeida-PalhaLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
Nuno SousaLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal. njcsousa@ecsaude.uminho.pt.
João J CerqueiraLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057, Braga, Portugal.
University of Minho · PTMax Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic stress is associated with increased risk of glucose intolerance and cardiovascular diseases, albeit through undefined mechanisms. With the aim of gaining insights into the latter, this study examined the metabolic profile of young adult male rats that were exposed to chronic unpredictable stress.

methodsYoung adult male rats were submitted to 4 weeks of chronic unpredictable stress and allowed to recover for 5 weeks. An extensive analysis including of morphologic, biochemical and molecular parameters was carried out both after chronic unpredictable stress and after recovery from stress.

resultsAfter 28 days of chronic unpredictable stress (CUS) the animals submitted to this protocol displayed less weight gain than control animals. After 5 weeks of recovery the weight gain rebounded to similar values of controls. In addition, following CUS, fasting insulin levels were increased and were accompanied by signs of impaired glucose tolerance and elevated serum corticosteroid levels. This biochemical profile persisted into the post-stress recovery period, despite the restoration of baseline corticosteroid levels. The mRNA expression levels of peroxisome proliferator-activated receptor (PPAR)-γ and lipocalin-2 in white adipose tissue were, respectively, down- and up-regulated.

conclusionsReduction of PPAR-γ expression and generation of a pro-inflammatory environment by increased lipocalin-2 expression in white adipose tissue may contribute to stress-induced glucose intolerance.

Indexed as

AnimalsBiomarkersBlood GlucoseChronic DiseaseCorticosteroneDisease Models, AnimalDown-RegulationGlucose IntoleranceInflammation MediatorsInsulinIntra-Abdominal FatLipocalin-2MalePhenotypePPAR gammaRats, WistarBiomarkersBlood GlucoseCorticosteroneInflammation MediatorsInsulinLcn2 protein, ratLipocalin-2PPAR gammaPPAR gamma, ratChronic unpredictable stressGlucose intoleranceLipocalin-2Metabolic syndromePPARWhite adipose tissue

Identifiers

PMID27538526
PMCPMC4990862
OpenAlexW2515343123

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.