Evidence map›Paper›PMID 28437656›Full record

ArticleRedox biology2017

A gene-environment interaction analysis of plasma selenium with prevalent and incident diabetes: The Hortega study.

Inmaculada Galan-Chilet, Maria Grau-Perez, Griselda De Marco, Eliseo Guallar, Juan Carlos Martin-Escudero, Alejandro Dominguez-Lucas, Isabel Gonzalez-Manzano, Raul Lopez-Izquierdo, Laisa Socorro Briongos-Figuero, Josep Redon and 2 more

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

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 4 pooled it
3.2field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 4 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  4. Selenium for preventing cancer.The Cochrane database of systematic reviews · 2018
    Pooled it
  5. Article
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  7. Review
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  12. Scientific opinion on the tolerable upper intake level for selenium.EFSA journal. European Food Safety Authority · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Selenium Status and Its Antioxidant Role in Metabolic Diseases.Oxidative medicine and cellular longevity · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 7 institutions in 2 countries.

Inmaculada Galan-ChiletGenomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain.
Maria Grau-PerezArea of Cardiometabolic and Renal Risk, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; Department of Environmental Health Sciences, Columbia University, New York, NY, USA; Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Griselda De MarcoGenomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain.
Eliseo GuallarDepartment of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Juan Carlos Martin-EscuderoDepartment of Internal Medicine, University Hospital Rio Hortega, Valladolid, Spain.
Alejandro Dominguez-LucasArea of Cardiometabolic and Renal Risk, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain.
Isabel Gonzalez-ManzanoDepartment of Internal Medicine, University Hospital Rio Hortega, Valladolid, Spain.
Raul Lopez-IzquierdoDepartment of Internal Medicine, University Hospital Rio Hortega, Valladolid, Spain.
Laisa Socorro Briongos-FigueroDepartment of Internal Medicine, University Hospital Rio Hortega, Valladolid, Spain.
Josep RedonArea of Cardiometabolic and Renal Risk, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; CIBER of Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Department of Internal Medicine, University Hospital Clinic of Valencia, Valencia, Spain.
Felipe Javier ChavesGenomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Institute of Health Carlos III, Madrid, Spain. Electronic address: felipe.chaves@uv.es.
Maria Tellez-PlazaArea of Cardiometabolic and Renal Risk, Biomedical Research Institute Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Hospital Universitario Río Hortega · ESINCLIVA Health Research Institute · ESColumbia University · USInstituto de Salud Carlos III · ESJohns Hopkins Medicine · USJohns Hopkins University · USSpanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSelenium and single-nucleotide-polymorphisms in selenoprotein genes have been associated to diabetes. However, the interaction of selenium with genetic variation in diabetes and oxidative stress-related genes has not been evaluated as a potential determinant of diabetes risk.

methodsWe evaluated the cross-sectional and prospective associations of plasma selenium concentrations with type 2 diabetes, and the interaction of selenium concentrations with genetic variation in candidate polymorphisms, in a representative sample of 1452 men and women aged 18-85 years from Spain.

resultsThe geometric mean of plasma selenium levels in the study sample was 84.2µg/L. 120 participants had diabetes at baseline. Among diabetes-free participants who were not lost during the follow-up (N=1234), 75 developed diabetes over time. The multivariable adjusted odds ratios (95% confidence interval) for diabetes prevalence comparing the second and third to the first tertiles of plasma selenium levels were 1.80 (1.03, 3.14) and 1.97 (1.14, 3.41), respectively. The corresponding hazard ratios (95% CI) for diabetes incidence were 1.76 (0.96, 3.22) and 1.80 (0.98, 3.31), respectively. In addition, we observed significant interactions between selenium and polymorphisms in PPARGC1A, and in genes encoding mitochondrial proteins, such as BCS1L and SDHA, and suggestive interactions of selenium with other genes related to selenoproteins and redox metabolism.

conclusionsPlasma selenium was positively associated with prevalent and incident diabetes. While the statistical interactions of selenium with polymorphisms involved in regulation of redox and insulin signaling pathways provide biological plausibility to the positive associations of selenium with diabetes, further research is needed to elucidate the causal pathways underlying these associations.

Indexed as

Gene Regulatory NetworksAdultAgedAged, 80 and overATPases Associated with Diverse Cellular ActivitiesCross-Sectional StudiesDiabetes Mellitus, Type 2Electron Transport Complex IIElectron Transport Complex IIIFemaleGene-Environment InteractionHumansIncidenceMaleMiddle AgedOxidation-ReductionATPases Associated with Diverse Cellular ActivitiesBCS1L protein, humanElectron Transport Complex IIElectron Transport Complex IIIPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanSDHA protein, humanSelenium

Identifiers

PMID28437656
PMCPMC5403796
OpenAlexW2606851485

What Socratic 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 Socratic graph.