Evidence map›Paper›PMID 36362842›Full record

ArticleLife (Basel, Switzerland)2022

Glycine Effect on the Expression Profile of Orphan Receptors GPR21, GPR26, GPR39, GPR82 and GPR6 in a Model of Inflammation in 3T3-L1 Cells.

Rocío Alejandra Gutiérrez-Rojas, Karla Aidee Aguayo-Cerón, Cruz Vargas-De-León, Sandra Edith Cabrera-Becerra, Julio Cesar Almanza-Pérez, Fengyang Huang, Santiago Villafaña, Rodrigo Romero-Nava

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2022. 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
0.4field-weighted citation impact, top 41% 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, 7 citations in OpenAlex.

  1. Article
  2. Glycine: The Smallest Anti-Inflammatory Micronutrient.International journal of molecular sciences · 2023
    Review
  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

8 authors at 4 institutions in 1 country.

Rocío Alejandra Gutiérrez-RojasEscuela Nacional de Ciencias Biologicas del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Karla Aidee Aguayo-CerónLaboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Cruz Vargas-De-LeónLaboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.ORCID 0000-0001-9428-3619
Sandra Edith Cabrera-BecerraLaboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Julio Cesar Almanza-PérezLaboratorio de Farmacología, Departamento de Ciencias de la Salud, DCBS, Universidad Autónoma Metropolitana-Iztapalapa (UAM-I), Ciudad de México 09340, Mexico.ORCID 0000-0002-9417-5500
Fengyang HuangLaboratorio de Investigación en Farmacología, Hospital Infantil de México Federico Gómez (HIMFG), Ciudad de México 06720, Mexico.ORCID 0000-0002-6503-694X
Santiago VillafañaLaboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Rodrigo Romero-NavaLaboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Instituto Politécnico Nacional · MXHospital Infantil de México Federico Gómez · MXHospital Juárez de México · MXUniversidad Autónoma Metropolitana · MX

Funding

Instituto Politécnico Nacional SIP-IPN-20220695
6 · The paper itself

Abstract

backgroundChronic or low-grade inflammation is a process where various immune cells are recruited from the periphery into adipose tissue. This event gives rise to localised inflammation, in addition to having a close interaction with cardiometabolic pathologies where the mediation of orphan receptors is observed. The aim of this study was to analyse the participation of the orphan receptors GPR21, GPR39, GPR82 and GPR6 in a chronic inflammatory process in 3T3-L1 cells. The 3T3-L1 cells were stimulated with TNF-α (5 ng/mL) for 60 min as an inflammatory model. Gene expression was measured by RT-qPCR.

resultsWe showed that the inflammatory stimulus of TNF-α in adipocytes decreased the expression of the orphan receptors GPR21, GPR26, GPR39, GPR82 and GPR6, which are related to low-grade inflammation.

conclusionsOur results suggest that GPR21 and GPR82 are modulated by glycine, it shows a possible protective role in the presence of an inflammatory environment in adipocytes, and they could be a therapeutic target to decrease the inflammation in some diseases related to low-grade inflammation such as diabetes, obesity and metabolic syndrome.

Indexed as

adipokinesglycineinflammationorphan receptors

Identifiers

PMID36362842
PMCPMC9696036
OpenAlexW4307262227

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.