Evidence map›Paper›PMID 32793223›Full record

ReviewFrontiers in immunology2020

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System.

Gholamreza Daryabor, Mohamad Reza Atashzar, Dieter Kabelitz, Seppo Meri, Kurosh Kalantar

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 287 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
287citing papers in PubMed, 10 pooled it
39.6field-weighted citation impact, top 1% 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

287 citing papers in PubMed, 10 syntheses or guidelines pooled it, 542 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Hypoglycemic activity ofFrontiers in pharmacology · 2024
    Pooled it
  8. Pooled it
  9. Pooled it
  10. Pooled it
  11. Trial
  12. Trial
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

227 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 3 countries.

Gholamreza DaryaborAutoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Mohamad Reza AtashzarDepartment of Immunology, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran.
Dieter KabelitzInstitute of Immunology, University of Kiel, Kiel, Germany.
Seppo MeriDepartment of Bacteriology and Immunology and the Translational Immunology Research Program (TRIMM), The University of Helsinki and HUSLAB, Helsinki University Hospital, Helsinki, Finland.
Kurosh KalantarDepartment of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz University of Medical Sciences · IRFasa University of Medical Sciences · IRKiel University · DEUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic abnormalities such as dyslipidemia, hyperinsulinemia, or insulin resistance and obesity play key roles in the induction and progression of type 2 diabetes mellitus (T2DM). The field of immunometabolism implies a bidirectional link between the immune system and metabolism, in which inflammation plays an essential role in the promotion of metabolic abnormalities (e.g., obesity and T2DM), and metabolic factors, in turn, regulate immune cell functions. Obesity as the main inducer of a systemic low-level inflammation is a main susceptibility factor for T2DM. Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. Hyperglycemia and the subsequent inflammation are the main causes of micro- and macroangiopathies in the circulatory system. They also promote the gut microbiota dysbiosis, increased intestinal permeability, and fatty liver disease. The impaired immune system together with metabolic imbalance also increases the susceptibility of patients to several pathogenic agents such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thus, the need for a proper immunization protocol among such patients is granted. The focus of the current review is to explore metabolic and immunological abnormalities affecting several organs of T2DM patients and explain the mechanisms, whereby diabetic patients become more susceptible to infectious diseases.

Indexed as

BetacoronavirusCoronavirus InfectionsCOVID-19Diabetes Mellitus, Type 2Disease SusceptibilityDysbiosisGastrointestinal MicrobiomeHumansHyperglycemiaImmune SystemInflammationMetabolic SyndromeObesityOxidative StressPandemicsPneumonia, Viralimmunometabolisminfectious diseasesinsulin resistanceobesitySARS-CoV-2systemic low-level inflammationtype 2 diabetes mellitus

Identifiers

PMID32793223
PMCPMC7387426
OpenAlexW3044728581

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.