Liver-specific RORα deletion does not affect the metabolic susceptibility to western style diet feeding.
Adipose Tissue, White
/ metabolism
Adiposity
/ genetics
Animals
Diet, Vegetarian
Diet, Western
Female
Gene Knockout Techniques
Glucose
/ metabolism
Hepatocytes
/ metabolism
Insulin Resistance
/ genetics
Lipid Metabolism
/ genetics
Liver
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Nuclear Receptor Subfamily 1, Group F, Member 1
/ genetics
Obesity
/ metabolism
Glucose metabolism
Obesity
RORα
Steatosis
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
09
01
2019
revised:
21
02
2019
accepted:
28
02
2019
pubmed:
25
3
2019
medline:
6
5
2020
entrez:
25
3
2019
Statut:
ppublish
Résumé
The nuclear receptor superfamily is a potential target for the development of new treatments for obesity and metabolic diseases. Increasing evidence has pointed towards the retinoic acid-related orphan receptor-alpha (RORα) as an important nuclear receptor involved in several biological processes. RORα full body knockout mice display improved metabolic phenotypes on both chow and high fat (60% fat, 20% carbohydrate) diets, but also have severe behavioral abnormalities. Here we investigated the effect of hepatic RORα by generating mice with liver-specific RORα deletion to elucidate the role of this nuclear receptor on host metabolism. 8 week-old mice with liver-specific RORα deletion and littermate controls were fed either chow or western-style diets (40% fat, 40% carbohydrate) for 12 weeks. Metabolic phenotyping was performed at the end of the dietary intervention. Here, we show that hepatic RORα deletion does not affect the metabolic susceptibility to either chow or western-style diet in terms of glucose metabolism and adiposity. Our data indicate that liver deletion of RORα does not have a pivotal role in the regulation of hepatic glucose and lipid metabolism on chow or western-style diet.
Identifiants
pubmed: 30904385
pii: S2212-8778(19)30029-8
doi: 10.1016/j.molmet.2019.02.010
pmc: PMC6479759
pii:
doi:
Substances chimiques
Nuclear Receptor Subfamily 1, Group F, Member 1
0
Rora protein, mouse
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
82-87Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier GmbH.. All rights reserved.
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