Revealing the role of peroxisome proliferator-activated receptor β/δ in nonalcoholic fatty liver disease.


Journal

Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267

Informations de publication

Date de publication:
01 2021
Historique:
received: 05 06 2020
revised: 16 07 2020
accepted: 08 08 2020
pubmed: 19 8 2020
medline: 28 1 2021
entrez: 19 8 2020
Statut: ppublish

Résumé

Nonalcoholic fatty liver disease (NAFLD), a form of chronic liver disease that occurs in individuals with no significant alcohol abuse, has become an increasing concern for global health. NAFLD is defined as the presence of lipid deposits in hepatocytes and it ranges from hepatic steatosis (fatty liver) to steatohepatitis. Emerging data from both preclinical studies and clinical trials suggest that the peroxisome proliferator-activated receptor (PPAR)β/δ plays an important role in the control of carbohydrate and lipid metabolism in liver, and its activation might hinder the progression of NAFLD. Here, we review the latest information on the effects of PPARβ/δ on NAFLD, including its capacity to reduce lipogenesis, to alleviate inflammation and endoplasmic reticulum stress, to ameliorate insulin resistance, and to attenuate liver injury. Because of these effects, activation of hepatic PPARβ/δ through synthetic or natural ligands provides a promising therapeutic option for the management of NAFLD.

Identifiants

pubmed: 32810487
pii: S0026-0495(20)30206-7
doi: 10.1016/j.metabol.2020.154342
pii:
doi:

Substances chimiques

PPAR delta 0
PPAR-beta 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

154342

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors have no conflict of interest to declare.

Auteurs

Mohammad Zarei (M)

Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain; Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain.

David Aguilar-Recarte (D)

Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain; Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain.

Xavier Palomer (X)

Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain; Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain.

Manuel Vázquez-Carrera (M)

Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain; Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain. Electronic address: mvazquezcarrera@ub.edu.

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Classifications MeSH