Evidence map›Paper›PMID 35144052›Full record

ReviewRedox biology2022

The role of selenium in type-2 diabetes mellitus and its metabolic comorbidities.

Holger Steinbrenner, Leonidas H Duntas, Margaret P Rayman

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

Review in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 2 pooled it
21.7field-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

102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 199 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

42 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

3 authors at 3 institutions in 3 countries.

Holger SteinbrennerInstitute of Nutritional Sciences, Nutrigenomics Section, Friedrich Schiller University, Dornburger Str. 29, 07743, Jena, Germany.
Leonidas H DuntasEvgenideion Hospital, Unit of Endocrinology, Metabolism and Diabetes, University of Athens, 20 Papadiamantopoulou Str, 11520, Athens, Greece.
Margaret P RaymanDepartment of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK. Electronic address: m.rayman@surrey.ac.uk.
Friedrich Schiller University Jena · DENational and Kapodistrian University of Athens · GRUniversity of Surrey · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review addresses the role of the essential trace element, selenium, in type-2 diabetes mellitus (T2DM) and its metabolic co-morbidities, i.e., metabolic syndrome, obesity and non-alcoholic fatty liver disease. We refer to the dietary requirements of selenium and the key physiological roles of selenoproteins. We explore the dysregulated fuel metabolism in T2DM and its co-morbidities, emphasizing the relevance of inflammation and oxidative stress. We describe the epidemiology of observational and experimental studies of selenium in diabetes and related conditions, explaining that the interaction between selenium status and glucose control is not limited to hyperglycemia but extends to hypoglycemia. We propose that the association between high plasma/serum selenium and T2DM/fasting plasma glucose observed in many cross-sectional studies may rely on the upregulation of hepatic selenoprotein-P biosynthesis in conditions of hyperglycemia and insulin resistance. While animal studies have revealed potential molecular mechanisms underlying adverse effects of severe selenium/selenoprotein excess and deficiency in the pathogenesis of insulin resistance and β-cell dysfunction, their translational significance is rather limited. Importantly, dietary selenium supplementation does not appear to be a major causal factor for the development of T2DM in humans though we cannot currently exclude a small contribution of selenium on top of other risk factors, in particular if it is ingested at high (supranutritional) doses. Elevated selenium biomarkers that are often measured in T2DM patients are more likely to be a consequence, rather than a cause, of diabetes.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceSeleniumAnimalsCross-Sectional StudiesHumansSelenoproteinsSeleniumSelenoproteinsDiabetesGlucoseHyperglycemiaHypoglycemiaMetabolic syndromeNAFLDObesitySeleniumβ-cell

Identifiers

PMID35144052
PMCPMC8844812
OpenAlexW4207018563

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.