Activation of NPRs and UCP1-independent pathway following CB1R antagonist treatment is associated with adipose tissue beiging in fat-fed male dogs.
Adipose Tissue
/ drug effects
Adipose Tissue, Brown
/ drug effects
Adipose Tissue, White
/ drug effects
Animals
Diet, High-Fat
/ adverse effects
Dogs
Gene Expression
/ drug effects
Inflammation
/ pathology
Insulin Resistance
Male
Organelle Biogenesis
Receptor, Cannabinoid, CB1
/ antagonists & inhibitors
Receptors, Adrenergic, beta
/ drug effects
Receptors, Atrial Natriuretic Factor
/ drug effects
Rimonabant
/ pharmacology
Thermogenesis
/ drug effects
Uncoupling Protein 1
/ drug effects
Weight Loss
/ drug effects
CB1R antagonist
adipose tissue beiging
dogs
insulin resistance
Journal
American journal of physiology. Endocrinology and metabolism
ISSN: 1522-1555
Titre abrégé: Am J Physiol Endocrinol Metab
Pays: United States
ID NLM: 100901226
Informations de publication
Date de publication:
01 09 2019
01 09 2019
Historique:
pubmed:
27
6
2019
medline:
24
3
2020
entrez:
26
6
2019
Statut:
ppublish
Résumé
CB1 receptor (CB1R) antagonism improves the deleterious effects of a high-fat diet (HFD) by reducing body fat mass and adipocyte cell size. Previous studies demonstrated that the beneficial effects of the CB1R antagonist rimonabant (RIM) in white adipose tissue (WAT) are partially due to an increase of mitochondria numbers and upregulation thermogenesis markers, suggesting an induction of WAT beiging. However, the molecular mechanism by which CB1R antagonism induces weight loss and WAT beiging is unclear. In this study, we probed for genes associated with beiging and explored longitudinal molecular mechanisms by which the beiging process occurs. HFD dogs received either RIM (HFD+RIM) or placebo (PL) (HFD+PL) for 16 wk. Several genes involved in beiging were increased in HFD+RIM compared with pre-fat, HFD, and HFD+PL. We evaluated lipolysis and its regulators including natriuretic peptide (NP) and its receptors (
Identifiants
pubmed: 31237449
doi: 10.1152/ajpendo.00539.2018
pmc: PMC6766608
doi:
Substances chimiques
Receptor, Cannabinoid, CB1
0
Receptors, Adrenergic, beta
0
Uncoupling Protein 1
0
Receptors, Atrial Natriuretic Factor
EC 4.6.1.2
Rimonabant
RML78EN3XE
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
E535-E547Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK027619
Pays : United States
Organisme : NIDDK NIH HHS
ID : R37 DK027619
Pays : United States
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