Evidence map›Paper›PMID 32903422›Full record

ArticleFrontiers in cardiovascular medicine2020

Insulin Treatment Reduces Susceptibility to Atrial Fibrillation in Type 1 Diabetic Mice.

Zahra Maria, Allison R Campolo, Benjamin J Scherlag, Jerry W Ritchey, Véronique A Lacombe

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  7. Review
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  9. Article
  10. Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
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 3 institutions in 1 country.

Zahra MariaDepartment of Physiological Sciences, Oklahoma State University, Stillwater, OK, United States.
Allison R CampoloDepartment of Physiological Sciences, Oklahoma State University, Stillwater, OK, United States.
Benjamin J ScherlagDepartment of Internal Medicine, University of Oklahoma College of Medicine, Oklahoma City, OK, United States.
Jerry W RitcheyDepartment of Veterinary Pathobiology, Oklahoma State University, Stillwater, OK, United States.
Véronique A LacombeDepartment of Physiological Sciences, Oklahoma State University, Stillwater, OK, United States.
University of Oklahoma Health Sciences Center · USOklahoma State University · USUniversity of Oklahoma · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes has been identified as an independent risk factor for atrial fibrillation (AF), the most common chronic cardiac arrhythmia. Whether or not glucose and insulin disturbances observed during diabetes enhance arrhythmogenicity of the atria, potentially leading to AF, is not well-known. We hypothesized that insulin deficiency and impaired glucose transport provide a metabolic substrate for the development and maintenance of AF during diabetes. Transesophageal atrial pacing was used to induce AF in healthy, streptozotocin-induced insulin-deficient type 1 diabetic, and insulin-treated diabetic mice. Translocation of insulin-sensitive glucose transporters (GLUTs) to the atrial cell surface was measured using a biotinylated photolabeling assay in the perfused heart. Fibrosis and glycogen accumulation in the atrium were measured using histological analysis. Diabetic mice displayed mild hyperglycemia, increased duration and frequency of AF episodes vs. age-matched controls (e.g., AF duration: 19.7 ± 6.8 s vs. 1.8 ± 1.1 s, respectively,

Indexed as

arrhythmiasatriadiabetesglucose transportersglycogenmetabolism

Identifiers

PMID32903422
PMCPMC7434932
OpenAlexW3048716082

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.