Evidence mapPaperPMID 38398039Full record

ReviewBiomedicines2024

Unraveling the Link between Ιnsulin Resistance and Bronchial Asthma.

Konstantinos Bartziokas, Andriana I Papaioannou, Fotios Drakopanagiotakis, Evanthia Gouveri, Nikolaos Papanas, Paschalis Steiropoulos

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Observational
  12. Observational
  13. Review
  14. 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

6 authors at 3 institutions in 1 country.

Konstantinos BartziokasPrivate Pulmonologist, 42132 Trikala, Greece.ORCID 0000-0002-9657-3705
Andriana I Papaioannou1st University Department of Respiratory Medicine, "Sotiria" Hospital, National and Kapodistrian University of Athens, 15772 Athens, Greece.
Fotios DrakopanagiotakisDepartment of Pneumonology, Medical School, Democritus University of Thrace, 68100 Alexandroupolis, Greece.ORCID 0000-0003-4408-291X
Evanthia GouveriDiabetes Centre, 2nd Department of Internal Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece.
Nikolaos PapanasDiabetes Centre, 2nd Department of Internal Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece.ORCID 0000-0002-7320-785X
Paschalis SteiropoulosDepartment of Pneumonology, Medical School, Democritus University of Thrace, 68100 Alexandroupolis, Greece.ORCID 0000-0001-7121-6253
Democritus University of Thrace · GRe-Trikala (Greece) · GRNational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence from large epidemiological studies has shown that obesity may predispose to increased Th2 inflammation and increase the odds of developing asthma. On the other hand, there is growing evidence suggesting that metabolic dysregulation that occurs with obesity, and more specifically hyperglycemia and insulin resistance, may modify immune cell function and in some degree systemic inflammation. Insulin resistance seldom occurs on its own, and in most cases constitutes a clinical component of metabolic syndrome, along with central obesity and dyslipidemia. Despite that, in some cases, hyperinsulinemia associated with insulin resistance has proven to be a stronger risk factor than body mass in developing asthma. This finding has been supported by recent experimental studies showing that insulin resistance may contribute to airway remodeling, promotion of airway smooth muscle (ASM) contractility and proliferation, increase of airway hyper-responsiveness and release of pro-inflammatory mediators from adipose tissue. All these effects indicate the potential impact of hyperinsulinemia on airway structure and function, suggesting the presence of a specific asthma phenotype with insulin resistance. Epidemiologic studies have found that individuals with severe and uncontrolled asthma have a higher prevalence of glycemic dysfunction, whereas longitudinal studies have linked glycemic dysfunction to an increased risk of asthma exacerbations. Since the components of metabolic syndrome interact with one another so much, it is challenging to identify each one's specific role in asthma. This is why, over the last decade, additional studies have been conducted to determine whether treatment of type 2 diabetes mellitus affects comorbid asthma as shown by the incidence of asthma, asthma control and asthma-related exacerbations. The purpose of this review is to present the mechanism of action, and existing preclinical and clinical data, regarding the effect of insulin resistance in asthma.

Indexed as

antidiabetic drugsasthmainsulin resistancemetabolic dysfunctionobesity

Identifiers

PMID38398039
PMCPMC10887139
OpenAlexW4391882081

What Socratic 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 Socratic graph.