Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome.
FGF21
insulin
thyroid hormone
triglyceride
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
28 Dec 2023
28 Dec 2023
Historique:
received:
10
03
2023
revised:
20
12
2023
accepted:
27
12
2023
medline:
2
1
2024
pubmed:
2
1
2024
entrez:
30
12
2023
Statut:
aheadofprint
Résumé
Endothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome. Wild type (etb
Identifiants
pubmed: 38159882
pii: S2212-8778(23)00202-8
doi: 10.1016/j.molmet.2023.101868
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
101868Informations de copyright
Copyright © 2023 The Author(s). Published by Elsevier GmbH.. All rights reserved.