Evidence map›Paper›PMID 23867154›Full record

ReviewFree radical biology & medicine2013

Selenium and diabetes--evidence from animal studies.

Jun Zhou, Kaixun Huang, Xin Gen Lei

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

Review in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 6 pooled it
10.9field-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

83 citing papers in PubMed, 6 syntheses or guidelines pooled it, 200 citations in OpenAlex.

  1. Pooled it
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  5. Selenium for preventing cancer.The Cochrane database of systematic reviews · 2018
    Pooled it
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23 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 2 institutions in 2 countries.

Jun ZhouHubei Key Laboratory of Bioinorganic Chemistry and Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan 430074, China.
Kaixun HuangHubei Key Laboratory of Bioinorganic Chemistry and Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan 430074, China.
Xin Gen LeiDepartment of Animal Science, Cornell University, Ithaca, NY 14853, USA. Electronic address: XL20@cornell.edu.
Huazhong University of Science and Technology · CNCornell University · US

Funding

ANTIOXIDATIVE ROLE OF GPX1 IN VIVO OF TRANSGENIC MICER01DK053018 · NIDDK · CORNELL UNIVERSITY ITHACA · PI LEI, XINGEN · 1997 to 2013
$2.8M
NIDDK NIH HHS DK53018NIDDK NIH HHS R01 DK053018
6 · The paper itself

Abstract

Whereas selenium was found to act as an insulin mimic and to be antidiabetic in earlier studies, recent animal experiments and human trials have shown an unexpected risk of prolonged high Se intake in potentiating insulin resistance and type 2 diabetes. Elevating dietary Se intake (0.4 to 3.0mg/kg of diet) above the nutrient requirements, similar to overproduction of selenoproteins, led to insulin resistance and/or diabetes-like phenotypes in mice, rats, and pigs. Although its diabetogenic mechanism remains unclear, high Se intake elevated activity or production of selenoproteins including GPx1, MsrB1, SelS, and SelP. This upregulation diminished intracellular reactive oxygen species and then dysregulated key regulators of β cells and insulin synthesis and secretion, leading to chronic hyperinsulinemia. Overscavenging intracellular H2O2 also attenuated oxidative inhibition of protein tyrosine phosphatases and suppressed insulin signaling. High Se intake might affect expression and/or function of key regulators of glycolysis, gluconeogenesis, and lipogenesis. Future research is needed to find out if certain forms of Se metabolites in addition to selenoproteins and if mechanisms other than intracellular redox control mediate the diabetogenic effects of high Se intake. Furthermore, a potential interactive role of high Se intake in the interphase of carcinogenesis and diabetogenesis should be explored to make optimal use of Se in human nutrition and health.

Indexed as

HyperinsulinismInsulin ResistanceAnimalsDiabetes Mellitus, Type 2GluconeogenesisGlycolysisHydrogen PeroxideInsulinInsulin SecretionLipogenesisMiceOxidation-ReductionRatsSeleniumSelenoproteinsSignal TransductionHydrogen PeroxideInsulinSeleniumSelenoproteinsadenosine monophosphate-activated protein kinaseAKTAMPKbasal dietBDDiabetesforkhead boxFOXFree radicalsglucose-stimulated insulin secretionglutathione peroxidase 1GPx1GSISH3H4HbA(1c)hemoglobin A(1c)histone 3histone 4InsrInsulininsulin receptorinsulin receptor substrateIRIRSknockoutKOmethionine-R-sulfoxide reductase 1MsrB1NPCNutritional Prevention of CancerOEoverexpressingpancreatic duodenal homeobox 1PDX1peroxisomal proliferator-activated receptor-γ coactivator 1αPGC-1αphosphatase with tensin homologyphosphatidylinositol 3-kinasephosphotyrosine phosphatasePI3-Kprotein kinase Bprotein tyrosine phosphatase 1bPTENPTP1bPTPasereactive oxygen speciesReactive oxygen speciesROSSclySelSELECTSeleniumSelenium and Vitamin E Cancer Prevention Trialselenocysteine lyaseselenoproteinSelenoproteinSODSREBP-1csterol regulatory element-binding protein-1csuperoxide dismutasethioredoxin reductaseTrxRUCP2uncoupling protein 2wild typeWT

Identifiers

PMID23867154
PMCPMC3859733
OpenAlexW2002711930

What OpenQuestion holds

Textmetadata
LicenceTDM
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.