Pharmacological PPARβ/δ activation upregulates VLDLR in hepatocytes.

Détails

ID Serval
serval:BIB_A4CE277BEFB1
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Pharmacological PPARβ/δ activation upregulates VLDLR in hepatocytes.
Périodique
Clinica e investigacion en arteriosclerosis
Auteur(s)
Zarei M., Barroso E., Palomer X., Escolà-Gil J.C., Cedó L., Wahli W., Vázquez-Carrera M.
ISSN
1578-1879 (Electronic)
ISSN-L
0214-9168
Statut éditorial
Publié
Date de publication
2019
Peer-reviewed
Oui
Volume
31
Numéro
3
Pages
111-118
Langue
anglais espagnol
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
The very low-density lipoprotein receptor (VLDLR) plays an important function in the control of serum triglycerides and in the development of non-alcoholic fatty liver disease (NAFLD). In this study, we investigated the role of peroxisome proliferator-activated receptor (PPAR)β/δ activation in hepatic VLDLR regulation. Treatment of mice fed a high-fat diet with the PPARβ/δ agonist GW501516 increased the hepatic expression of Vldlr. Similarly, exposure of human Huh-7 hepatocytes to GW501516 increased the expression of VLDLR and triglyceride accumulation, the latter being prevented by VLDLR knockdown. Finally, treatment with another PPARβ/δ agonist increased VLDLR levels in the liver of wild-type mice, but not PPARβ/δ-deficient mice, confirming the regulation of hepatic VLDLR by this nuclear receptor. Our results suggest that upregulation of hepatic VLDLR by PPARβ/δ agonists might contribute to the hypolipidemic effect of these drugs by increasing lipoprotein delivery to the liver. Overall, these findings provide new effects by which PPARβ/δ regulate VLDLR levels and may influence serum triglyceride levels and NAFLD development.
Mots-clé
EHGNA, NAFLD, PPAR, VLDLR
Pubmed
Web of science
Création de la notice
28/04/2019 15:44
Dernière modification de la notice
21/08/2019 6:37
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