Evidence map›Paper›PMID 27421726›Full record

ArticleDiabetologia2016

LIGHT/TNFSF14 is increased in patients with type 2 diabetes mellitus and promotes islet cell dysfunction and endothelial cell inflammation in vitro.

Bente Halvorsen, Francesca Santilli, Hanne Scholz, Afaf Sahraoui, Hanne L Gulseth, Cecilie Wium, Stefano Lattanzio, Gloria Formoso, Patrizia Di Fulvio, Kari Otterdal and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 62 citations in OpenAlex.

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  10. LIGHT Amplification by NF-Mediators of inflammation · 2023
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  11. NClinical and translational medicine · 2023
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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

20 authors at 3 institutions in 2 countries.

Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway. bente.halvorsen@rr-research.no.
Francesca SantilliCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Hanne ScholzInstitute for Surgical Research, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Afaf SahraouiInstitute for Surgical Research, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Hanne L GulsethDepartment of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Cecilie WiumDepartment of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Stefano LattanzioCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Gloria FormosoCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Patrizia Di FulvioCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Kari OtterdalResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Kjetil RetterstølLipid Clinic, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Kirsten B HolvenDepartment of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Ida GregersenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Benedicte StavikResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Vigdis BjerkeliResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Rossella LianiCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Giovanni DaviCenter of Excellence on Aging, University of Chieti, Chieti, Italy.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Oslo University Hospital · NOUniversity of Chieti-Pescara · ITUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisActivation of inflammatory pathways is involved in the pathogenesis of type 2 diabetes mellitus. On the basis of its role in vascular inflammation and in metabolic disorders, we hypothesised that the TNF superfamily (TNFSF) member 14 (LIGHT/TNFSF14) could be involved in the pathogenesis of type 2 diabetes mellitus.

methodsPlasma levels of LIGHT were measured in two cohorts of type 2 diabetes mellitus patients (191 Italian and 40 Norwegian). Human pancreatic islet cells and arterial endothelial cells were used to explore regulation and relevant effects of LIGHT in vitro.

resultsOur major findings were: (1) in both diabetic cohorts, plasma levels of LIGHT were significantly raised compared with sex- and age-matched healthy controls (n = 32); (2) enhanced release from activated platelets seems to be an important contributor to the raised LIGHT levels in type 2 diabetes mellitus; (3) in human pancreatic islet cells, inflammatory cytokines increased the release of LIGHT and upregulated mRNA and protein levels of the LIGHT receptors lymphotoxin β receptor (LTβR) and TNF receptor superfamily member 14 (HVEM/TNFRSF14); (4) in these cells, LIGHT attenuated the insulin release in response to high glucose at least partly via pro-apoptotic effects; and (5) in human arterial endothelial cells, glucose boosted inflammatory response to LIGHT, accompanied by an upregulation of mRNA levels of HVEM (also known as TNFRSF14) and LTβR (also known as LTBR). CONCLUSIONS/

interpretationOur findings show that patients with type 2 diabetes mellitus are characterised by increased plasma LIGHT levels. Our in vitro findings suggest that LIGHT may contribute to the progression of type 2 diabetes mellitus by attenuating insulin secretion in pancreatic islet cells and by contributing to vascular inflammation.

Indexed as

AgedBlotting, WesternDiabetes Mellitus, Type 2Endothelial CellsFemaleHumansInflammationInsulinIslets of LangerhansLeukocytes, MononuclearLymphotoxin beta ReceptorMaleMiddle AgedReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTumor Necrosis Factor Ligand Superfamily Member 14InsulinLymphotoxin beta ReceptorRNA, MessengerTumor Necrosis Factor Ligand Superfamily Member 14CytokinesEndothelial cellsInflammationInsulinIsletsType 2 diabetes

Identifiers

PMID27421726
PMCPMC5016561
OpenAlexW2470733642

What OpenQuestion holds

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LicenceCC BY
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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.