The PPARβ/δ-AMPK Connection in the Treatment of Insulin Resistance.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_745478D849DF
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
The PPARβ/δ-AMPK Connection in the Treatment of Insulin Resistance.
Périodique
International journal of molecular sciences
Auteur⸱e⸱s
Aguilar-Recarte D., Palomer X., Wahli W., Vázquez-Carrera M.
ISSN
1422-0067 (Electronic)
ISSN-L
1422-0067
Statut éditorial
Publié
Date de publication
09/08/2021
Peer-reviewed
Oui
Volume
22
Numéro
16
Pages
8555
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: epublish
Résumé
The current treatment options for type 2 diabetes mellitus do not adequately control the disease in many patients. Consequently, there is a need for new drugs to prevent and treat type 2 diabetes mellitus. Among the new potential pharmacological strategies, activators of peroxisome proliferator-activated receptor (PPAR)β/δ show promise. Remarkably, most of the antidiabetic effects of PPARβ/δ agonists involve AMP-activated protein kinase (AMPK) activation. This review summarizes the recent mechanistic insights into the antidiabetic effects of the PPARβ/δ-AMPK pathway, including the upregulation of glucose uptake, muscle remodeling, enhanced fatty acid oxidation, and autophagy, as well as the inhibition of endoplasmic reticulum stress and inflammation. A better understanding of the mechanisms underlying the effects resulting from the PPARβ/δ-AMPK pathway may provide the basis for the development of new therapies in the prevention and treatment of insulin resistance and type 2 diabetes mellitus.
Mots-clé
AMPK, GDF15, PPARβ/δ, insulin resistance, type 2 diabetes mellitus
Pubmed
Web of science
Open Access
Oui
Création de la notice
03/09/2021 18:06
Dernière modification de la notice
12/01/2022 7:11
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