Modifications in GPR21 and GPR82 genes expression as a consequence of metabolic syndrome etiology.
Animals
Aorta
/ metabolism
Brain
/ metabolism
Diet
/ adverse effects
Gene Expression Regulation
/ genetics
Humans
Kidney
/ metabolism
Liver
/ metabolism
Metabolic Syndrome
/ etiology
Myocardium
/ metabolism
Obesity
/ genetics
Pancreas
/ injuries
Rats
Rats, Zucker
/ genetics
Receptors, G-Protein-Coupled
/ genetics
Triglycerides
/ blood
GPR21
GPR82
Metabolic syndrome
orphan receptors
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
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