Evidence map›Paper›PMID 29795582›Full record

ArticlePloS one2018

PKR modulates abnormal brain signaling in experimental obesity.

Mariko Taga, François Mouton-Liger, Malha Sadoune, Sarah Gourmaud, Jenny Norman, Marion Tible, Sylvie Thomasseau, Claire Paquet, James A R Nicoll, Delphine Boche and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mapping of Microglial Brain Region, Sex and Age Heterogeneity in Obesity.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. PKR: A Kinase to Remember.Frontiers in molecular neuroscience · 2018
    Review
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 3 institutions in 2 countries.

Mariko TagaClinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.ORCID 0000-0003-3780-7054
François Mouton-LigerINSERM Units U942, Paris, France.
Malha SadouneINSERM Units U942, Paris, France.
Sarah GourmaudINSERM Units U942, Paris, France.
Jenny NormanHistochemistry Research Unit, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Marion TibleINSERM Units U942, Paris, France.
Sylvie ThomasseauINSERM Units U942, Paris, France.
Claire PaquetINSERM Units U942, Paris, France.
James A R NicollClinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Delphine BocheClinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Jacques HugonINSERM Units U942, Paris, France.
Inserm · FRUniversity of Southampton · GBUniversity Hospital Southampton NHS Foundation Trust · GB

Funding

Medical Research Council G0900582
6 · The paper itself

Abstract

Metabolic disorders including obesity and type 2 diabetes are known to be associated with chronic inflammation and are obvious risk factors for Alzheimer's disease. Recent evidences concerning obesity and diabetes suggest that the metabolic inflammasome ("metaflammasome") mediates chronic inflammation. The double-stranded RNA-dependent protein kinase (PKR) is a central component of the metaflammasome. In wild type (WT) and PKR-/- mice, blood glucose, insulin and lipid levels and the brain expression of the phosphorylated components of the metaflammasome-PKR, JNK, IRS1 and IKKbeta-were studied after the induction of obesity by a high fat diet (HFD). The results showed significant increased levels of activated brain metaflammasome proteins in exposed WT mice but the changes were not significant in PKR-/- mice. In addition, gain weight was observed in WT mice and also in PKR-/- mice exposed to HFD. Increased blood insulin level was more accentuated in PKR -/- mice. The modulation of PKR activity could be an appropriate therapeutic approach, aimed at reducing abnormal brain metabolism and inflammation linked to metabolic disorders in order to reduce the risk of neurodegeneration.

Indexed as

AnimalsBlood GlucoseBrainCholesterol, HDLCholesterol, LDLDiet, High-FateIF-2 KinaseGene Expression RegulationGlucose Tolerance TestI-kappa B KinaseInflammationInsulinInsulin Receptor Substrate ProteinsMaleMAP Kinase Kinase 4MiceBlood GlucoseCholesterol, HDLCholesterol, LDLeIF-2 KinaseI-kappa B KinaseInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseMAP Kinase Kinase 4protein kinase R, mouseTriglycerides

Identifiers

PMID29795582
PMCPMC5968403
OpenAlexW2803406753

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.