Evidence map›Paper›PMID 31822562›Full record

ArticleThe Journal of biological chemistry2020

Distinct alterations of gut morphology and microbiota characterize accelerated diabetes onset in nonobese diabetic mice.

Marie-Christine Simon, Anna Lena Reinbeck, Corinna Wessel, Julia Heindirk, Tomas Jelenik, Kirti Kaul, Juan Arreguin-Cano, Alexander Strom, Michael Blaut, Fredrik Bäckhed and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Advances in fecal microbiota transplantation for the treatment of diabetes mellitus.Frontiers in cellular and infection microbiology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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

12 authors at 5 institutions in 3 countries.

Marie-Christine SimonInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Anna Lena ReinbeckInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Corinna WesselInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Julia HeindirkInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Tomas JelenikInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Kirti KaulInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Juan Arreguin-CanoInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Alexander StromInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Michael BlautDepartment of Gastrointestinal Microbiology, German Institute of Human Nutrition, D-14558 Potsdam-Rehbrücke, Germany.
Fredrik BäckhedWallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, S-41348 Gothenburg, Sweden.
Volker BurkartInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
Michael RodenInstitute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany michael.roden@ddz.de.
Deutsches Diabetes-Zentrum e.V. · DEGerman Center for Diabetes Research · DEHeinrich Heine University Düsseldorf · DEGerman Institute of Human Nutrition · DEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The rising prevalence of type 1 diabetes (T1D) over the past decades has been linked to lifestyle changes, but the underlying mechanisms are largely unknown. Recent findings point to gut-associated mechanisms in the control of T1D pathogenesis. In nonobese diabetic (NOD) mice, a model of T1D, diabetes development accelerates after deletion of the Toll-like receptor 4 (TLR4). We hypothesized that altered intestinal functions contribute to metabolic alterations, which favor accelerated diabetes development in TLR4-deficient (TLR4

Indexed as

Gastrointestinal Microbiomealpha-2-HS-GlycoproteinAnimalsBlood GlucoseBody WeightDiabetes Mellitus, ExperimentalEnergy MetabolismFatty AcidsGastrointestinal TractHomeostasisLipopolysaccharidesLiverMice, Inbred C57BLMice, Inbred NODModels, BiologicalOxidation-Reductionalpha-2-HS-GlycoproteinBlood GlucoseFatty AcidsLipopolysaccharidesTlr4 protein, mouseToll-Like Receptor 4animal modelautoimmune diseaseglucose metabolisminsulin resistanceisletmicrobiomemitochondrial metabolismToll-like receptor 4 (TLR4)type 1 diabetes

Identifiers

PMID31822562
PMCPMC6983849
OpenAlexW2996567330

What OpenQuestion holds

Textmetadata
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.