Reversal of diet-induced hepatic steatosis by peripheral CB1 receptor blockade in mice is p53/miRNA-22/SIRT1/PPARα dependent.
Animals
Diet, High-Fat
Fatty Acids
/ metabolism
Fatty Liver
/ genetics
Hep G2 Cells
Hepatocytes
/ metabolism
Humans
Lipid Metabolism
/ physiology
Lipids
/ physiology
Liver
/ metabolism
Male
Mice
Mice, Inbred C57BL
MicroRNAs
/ genetics
Obesity
/ metabolism
Oxidation-Reduction
PPAR alpha
/ metabolism
Phylogeny
Receptor, Cannabinoid, CB1
/ antagonists & inhibitors
Signal Transduction
Sirtuin 1
/ metabolism
Tumor Suppressor Protein p53
/ metabolism
Endocannabinoids
Fatty liver
Nuclear receptor
Obesity
microRNAs
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
19
05
2020
revised:
03
09
2020
accepted:
17
09
2020
pubmed:
29
9
2020
medline:
8
9
2021
entrez:
28
9
2020
Statut:
ppublish
Résumé
The endocannabinoid (eCB) system is increasingly recognized as being crucially important in obesity-related hepatic steatosis. By activating the hepatic cannabinoid-1 receptor (CB We combined unbiased bioinformatics techniques, mouse genetic manipulations, multiple pharmacological, molecular, and cellular biology approaches, and genomic sequencing to systematically decipher the role of the hepatic CB Using an unbiased normalized phylogenetic profiling analysis, we found that the CB We provide strong evidence for a functional role of the p53/miR-22/SIRT1/PPARα signaling pathway in potentially mediating the antisteatotic effect of peripherally restricted CB
Identifiants
pubmed: 32987186
pii: S2212-8778(20)30161-7
doi: 10.1016/j.molmet.2020.101087
pmc: PMC7563015
pii:
doi:
Substances chimiques
CNR1 protein, mouse
0
Fatty Acids
0
Lipids
0
MicroRNAs
0
Mirn22 microRNA, mouse
0
PPAR alpha
0
Receptor, Cannabinoid, CB1
0
Trp53 protein, mouse
0
Tumor Suppressor Protein p53
0
Sirt1 protein, mouse
EC 3.5.1.-
Sirtuin 1
EC 3.5.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101087Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier GmbH.. All rights reserved.
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