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
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

101868

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier GmbH.. All rights reserved.

Auteurs

Martina Feger (M)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Leonie Meier (L)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Jörg Strotmann (J)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Miriam Hoene (M)

Institute for Clinical Chemistry and Pathobiochemistry, Department for Diagnostic Laboratory Medicine, University Hospital Tübingen, Tübingen, Germany.

Julia Vogt (J)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Alexandra Wisser (A)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Susanna Hirschle (S)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Marie-Jo Kheim (MJ)

University of Hohenheim, Department of Physiology, Stuttgart, Germany.

Berthold Hocher (B)

University of Heidelberg, Department of Nephrology, Mannheim, Germany; Institute of Medical Diagnostics, IMD, Berlin, Germany; Clinical Research Center for Reproduction and Genetics in Hunan Province, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, Hunan, China.

Cora Weigert (C)

Institute for Clinical Chemistry and Pathobiochemistry, Department for Diagnostic Laboratory Medicine, University Hospital Tübingen, Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Zentrum München, University of Tübingen, Tübingen, Germany; German Center for Diabetes Research (DZD), 85784 Neuherberg, Germany.

Michael Föller (M)

University of Hohenheim, Department of Physiology, Stuttgart, Germany. Electronic address: michael.foeller@uni-hohenheim.de.

Classifications MeSH