Evidence map›Paper›PMID 34504172›Full record

ArticleScientific reports2021

TLR4-interactor with leucine-rich repeats (TRIL) is involved in diet-induced hypothalamic inflammation.

Alexandre Moura-Assis, Pedro A S Nogueira, Jose C de-Lima-Junior, Fernando M Simabuco, Joana M Gaspar, Jose Donato, Licio A Velloso

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Genomic Analysis of Inbreeding Depression on Productive Traits in Rubia Galega Beef Cattle Breed.Journal of animal breeding and genetics = Zeitschrift fur Tierzuchtung und Zuchtungsbiologie · 2026
    Article
  2. Article
  3. 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

7 authors at 2 institutions in 1 country.

Alexandre Moura-AssisLaboratory of Cell Signalling-Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil. amoura@rockefeller.edu.
Pedro A S NogueiraLaboratory of Cell Signalling-Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Jose C de-Lima-JuniorLaboratory of Cell Signalling-Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Fernando M SimabucoMultidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil.
Joana M GasparLaboratory of Cell Signalling-Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Jose DonatoDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Licio A VellosoLaboratory of Cell Signalling-Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil. lavellos@unicamp.br.
Universidade Estadual de Campinas (UNICAMP) · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and high-fat diet (HFD) consumption result in hypothalamic inflammation and metabolic dysfunction. While the TLR4 activation by dietary fats is a well-characterized pathway involved in the neuronal and glial inflammation, the role of its accessory proteins in diet-induced hypothalamic inflammation remains unknown. Here, we demonstrate that the knockdown of TLR4-interactor with leucine-rich repeats (Tril), a functional component of TLR4, resulted in reduced hypothalamic inflammation, increased whole-body energy expenditure, improved the systemic glucose tolerance and protection from diet-induced obesity. The POMC-specific knockdown of Tril resulted in decreased body fat, decreased white adipose tissue inflammation and a trend toward increased leptin signaling in POMC neurons. Thus, Tril was identified as a new component of the complex mechanisms that promote hypothalamic dysfunction in experimental obesity and its inhibition in the hypothalamus may represent a novel target for obesity treatment.

Indexed as

Adipose TissueAnimalsDiet, High-FatEnergy MetabolismGene Expression RegulationGlucose Tolerance TestHypothalamusInflammationIntercellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutNeuronsObesityIntercellular Signaling Peptides and ProteinsMembrane ProteinsPro-OpiomelanocortinRNA, MessengerTlr4 protein, mouseToll-Like Receptor 4Tril protein, mouse

Identifiers

PMID34504172
PMCPMC8429592
OpenAlexW3196961252

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.