Evidence map›Paper›PMID 31388695›Full record

ArticleDiabetologia2019

Genetic inactivation of the LIGHT (TNFSF14) cytokine in mice restores glucose homeostasis and diminishes hepatic steatosis.

Andrea Herrero-Cervera, Ángela Vinué, Deborah J Burks, Herminia González-Navarro

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Systemic Inflammation and Peripheral T Cell Responses Associate With Hepatic Energy Metabolism in Recent-Onset Type 1 Diabetes.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  2. Article
  3. Review
  4. LIGHT/TNFSF14 Affects Adipose Tissue Phenotype.International journal of molecular sciences · 2024
    Article
  5. Article
  6. High levels of LIGHT/TNFSF14 in patients with Prader-Willi syndrome.Journal of endocrinological investigation · 2023
    Article
  7. Article
  8. Review
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  11. Article
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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

4 authors at 2 institutions in 1 country.

Andrea Herrero-CerveraINCLIVA Health Research Institute, Avda. Menéndez Pelayo, 4, 46010, Valencia, Spain.
Ángela VinuéINCLIVA Health Research Institute, Avda. Menéndez Pelayo, 4, 46010, Valencia, Spain.
Deborah J BurksThe Prince Felipe Research Center (CIPF), Valencia, Spain.
Herminia González-NavarroINCLIVA Health Research Institute, Avda. Menéndez Pelayo, 4, 46010, Valencia, Spain. herminia.gonzalez@uv.es.
INCLIVA Health Research Institute · ESCentro de Investigacion Principe Felipe · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisNon-alcoholic fatty liver disease (NAFLD) is frequently associated with type 2 diabetes mellitus. Progression of NAFLD is mediated, among other things, by activation of inflammatory pathways. In the present study, the role of the proinflammatory cytokine LIGHT (TNFSF14) was explored in NAFLD and type 2 diabetes mellitus in mice deficient for the cytokine.

methodsLight-deficient (Light

resultsLight deficiency did not have an effect on metabolism, in NAFL or in tissue and systemic inflammation, in RCD-fed WT mice. HVEM and LTβR were markedly increased in livers of HFHCD-fed WT mice compared with RCD-fed WT controls. In WT mice under HFHCD, Light deficiency improved glucose tolerance and insulin sensitivity. Non-alcoholic fatty liver disease activity (NAS) score, hepatic CD3 CONCLUSIONS/

interpretationThese results indicate that Light deficiency in HFHCD improves hepatic glucose tolerance, and reduces hepatic inflammation and NAFL. This is accompanied by decreased systemic inflammation and adipose tissue cytokine secretion and by changes in the expression of key genes such as Klf6 and Tlr4 involved in NAFLD. These results suggest that therapies to block LIGHT-dependent signalling might be useful to restore hepatic homeostasis and to restrain NAFLD.

Indexed as

Adipose TissueAnimalsBlood GlucoseBody WeightConstriction, PathologicCytokinesDiabetes Mellitus, Type 2Disease ProgressionFatty LiverFemaleHomeostasisInflammationKruppel-Like Factor 6LiverMaleMiceBlood GlucoseCytokinesKlf6 protein, mouseKruppel-Like Factor 6Tlr4 protein, mouseTnfsf14 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor Ligand Superfamily Member 14Adipose tissueGlucose intoleranceHepatic steatosisInsulin resistanceLIGHT (TNFSF14)Metabolism

Identifiers

PMID31388695
OpenAlexW2966241365

What OpenQuestion holds

Textmetadata
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.