Evidence mapPaperPMID 30837889Full record

ReviewFrontiers in physiology2019

Heterogeneity of Metabolic Defects in Type 2 Diabetes and Its Relation to Reactive Oxygen Species and Alterations in Beta-Cell Mass.

Andris Elksnis, Mats Martinell, Olof Eriksson, Daniel Espes

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04053621 (Pirofosfato de Tiamina Como Coadyuvante de la Metformina en el Tratamiento de Pacientes Con Diabetes Mellitus Tipo 2), which is not on this map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.6field-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.

NCT04053621 naunknown statusstarted 2021, after this paper: background citation

Pirofosfato de Tiamina Como Coadyuvante de la Metformina en el Tratamiento de Pacientes Con Diabetes Mellitus Tipo 2

Ran2021Enrolled92Registered outcomes7Posted comparisons0ConditionsDiabetes Mellitus, Type 2ArmsMetformin, Placebo, Thiamine pyrophosphate
Open the trial in the graph
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Histologic and Biochemical Effect ofEthiopian journal of health sciences · 2023
    Article
  12. Article
  13. Dysregulated UPR and ER Stress Related to a Mutation in theInternational journal of molecular sciences · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Nrf2: The Master and Captain of Beta Cell Fate.Trends in endocrinology and metabolism: TEM · 2021
    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

4 authors at 2 institutions in 1 country.

Andris ElksnisDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Mats MartinellDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Olof ErikssonScience for Life Laboratory, Department of Medicinal Chemistry, Uppsala University, Uppsala, Sweden.
Daniel EspesDepartment of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Uppsala University · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is a complex and heterogeneous disease which affects millions of people worldwide. The classification of diabetes is at an interesting turning point and there have been several recent reports on sub-classification of T2D based on phenotypical and metabolic characteristics. An important, and perhaps so far underestimated, factor in the pathophysiology of T2D is the role of oxidative stress and reactive oxygen species (ROS). There are multiple pathways for excessive ROS formation in T2D and in addition, beta-cells have an inherent deficit in the capacity to cope with oxidative stress. ROS formation could be causal, but also contribute to a large number of the metabolic defects in T2D, including beta-cell dysfunction and loss. Currently, our knowledge on beta-cell mass is limited to autopsy studies and based on comparisons with healthy controls. The combined evidence suggests that beta-cell mass is unaltered at onset of T2D but that it declines progressively. In order to better understand the pathophysiology of T2D, to identify and evaluate novel treatments, there is a need for

Indexed as

beta-cellbeta-cell massdiabetes classificationimagingoxygen stresspositron emission tomographyreactive oxygen speciestype 2 diabetes

Identifiers

PMID30837889
PMCPMC6383038
OpenAlexW2912566998

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.