Modifications in GPR21 and GPR82 genes expression as a consequence of metabolic syndrome etiology.


Journal

Journal of receptor and signal transduction research
ISSN: 1532-4281
Titre abrégé: J Recept Signal Transduct Res
Pays: England
ID NLM: 9509432

Informations de publication

Date de publication:
Feb 2021
Historique:
pubmed: 26 6 2020
medline: 5 10 2021
entrez: 26 6 2020
Statut: ppublish

Résumé

Metabolic syndrome (MS) has been related with alterations in expression levels of orphan G protein coupled receptors (GPCRs) such as GPR21 and GPR82, which could be involved in some of the elements that characterizes the metabolic syndrome. The aim of this work was to evaluate changes in GPR21 and GPR82 receptors expression in two models of metabolic syndrome: one genetic (Zucker rats), and the other based on a diet (70% fructose for 9 weeks). GPR21 and GPR82 gene expressions were evaluated in brain, heart, aorta, liver and kidney by RT-qPCR. Rats with a high fructose diet, as well as obese Zucker rats, showed initial stages of pancreatic damage and alterations in some biochemical parameters related to the model consistent with the classification of MS. GPR21 and GPR82 receptors expressed in all tissues. The expression of GPR21 decreased in heart, aorta and kidney, but in liver the expression was different: decreased in diet model and increased in genetic model. In contrast, GPR82 expression depended of tissue and metabolic syndrome model. The results highlight the possible role of GPR21 and GPR82 receptors in the development MS. We conclude that the expression of GPR21 and GPR82 in different tissues is related with MS and depend of the origin of the syndrome, so they could be a therapeutic target for that syndrome.

Identifiants

pubmed: 32583711
doi: 10.1080/10799893.2020.1784228
doi:

Substances chimiques

GPR21 protein, human 0
Receptors, G-Protein-Coupled 0
Triglycerides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

38-44

Auteurs

Rodrigo Romero-Nava (R)

Laboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México, México.
Laboratorio de Investigación en Farmacología, Hospital Infantil de México Federico Gómez (HIMFG), Ciudad de México, México.

Noemí García (N)

Escuela Nacional de Medicina, Tecnológico de Monterrey, Monterrey, México.

Karla Aidee Aguayo-Cerón (KA)

Laboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México, México.

Fausto Sánchez Muñoz (F)

Departamento de Inmunología, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, México.

Fengyang Huang (F)

Laboratorio de Investigación en Farmacología, Hospital Infantil de México Federico Gómez (HIMFG), Ciudad de México, México.

Enrique Hong (E)

Departamento de Neurofarmacobiología, Centro de Investigación y de Estudios Avanzados, Ciudad de México, México.

Santiago Villafaña (S)

Laboratorio de Señalización Intracelular, Sección de Estudios de Posgrado, Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México, México.

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Classifications MeSH