Dietary nitrate attenuates high-fat diet-induced obesity via mechanisms involving higher adipocyte respiration and alterations in inflammatory status.
Adipocytes
/ cytology
Animals
Blood Glucose
/ drug effects
Cell Respiration
/ drug effects
Diet, High-Fat
/ adverse effects
Disease Models, Animal
Gene Expression Regulation
/ drug effects
Male
Membrane Transport Proteins
/ metabolism
Mice, Inbred C57BL
Mitochondria
/ drug effects
Nitrates
/ administration & dosage
Obesity
/ chemically induced
Palmitic Acid
/ adverse effects
Random Allocation
Uncoupling Protein 1
/ metabolism
Up-Regulation
Inflammation
Inorganic nitrate
Metabolic syndrome
Mitochondria
Thermogenesis
Visceral fat
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
07
10
2019
revised:
11
11
2019
accepted:
13
11
2019
pubmed:
26
11
2019
medline:
2
10
2020
entrez:
26
11
2019
Statut:
ppublish
Résumé
Emerging evidence indicates that dietary nitrate can reverse several features of the metabolic syndrome, but the underlying molecular mechanisms still remain elusive. The aim of the present study was to explore mechanisms involved in the effects of dietary nitrate on the metabolic dysfunctions induced by high-fat diet (HFD) in mice. Four weeks old C57BL/6 male mice, exposed to HFD for ten weeks, were characterised by increased body weight, fat content, increased fasting glucose and impaired glucose clearance. All these metabolic abnormalities were significantly attenuated by dietary nitrate. Mechanistically, subcutaneous primary mouse adipocytes exposed to palmitate (PA) and treated with nitrite exhibited higher mitochondrial respiration, increased protein expression of total mitochondrial complexes and elevated gene expression of the thermogenesis gene UCP-1, as well as of the creatine transporter SLC6A8. Finally, dietary nitrate increased the expression of anti-inflammatory markers in visceral fat, plasma and bone marrow-derived macrophages (Arginase-1, Egr-2, IL-10), which was associated with reduction of NADPH oxidase-derived superoxide production in macrophages. In conclusion, dietary nitrate may have therapeutic utility against obesity and associated metabolic complications possibly by increasing adipocyte mitochondrial respiration and by dampening inflammation and oxidative stress.
Identifiants
pubmed: 31765889
pii: S2213-2317(19)31220-0
doi: 10.1016/j.redox.2019.101387
pmc: PMC6883295
pii:
doi:
Substances chimiques
Blood Glucose
0
Membrane Transport Proteins
0
Nitrates
0
Ucp1 protein, mouse
0
Uncoupling Protein 1
0
creatine transporter
0
Palmitic Acid
2V16EO95H1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101387Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.
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