Nitrate consumption preserves HFD-induced skeletal muscle mitochondrial ADP sensitivity and lysine acetylation: A potential role for SIRT1.
AMP-Activated Protein Kinases
/ genetics
Acetylation
Adenosine Diphosphate
/ metabolism
Animals
Diet, High-Fat
/ adverse effects
Glucose
/ metabolism
Insulin
/ metabolism
Insulin Resistance
Lysine
/ metabolism
Mice
Mice, Inbred C57BL
Muscle, Skeletal
/ metabolism
Nitrates
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
Sirtuin 1
/ genetics
Insulin resistance
Mitochondrial dysfunction
Nitrate
Obesity
SIRT1
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
12
03
2022
accepted:
28
03
2022
pubmed:
11
4
2022
medline:
11
5
2022
entrez:
10
4
2022
Statut:
ppublish
Résumé
Dietary nitrate supplementation, and the subsequent serial reduction to nitric oxide, has been shown to improve glucose homeostasis in several pre-clinical models of obesity and insulin resistance. While the mechanisms remain poorly defined, the beneficial effects of nitrate appear to be partially dependent on AMPK-mediated signaling events, a central regulator of metabolism and mitochondrial bioenergetics. Since AMPK can activate SIRT1, we aimed to determine if nitrate supplementation (4 mM sodium nitrate via drinking water) improved skeletal muscle mitochondrial bioenergetics and acetylation status in mice fed a high-fat diet (HFD: 60% fat). Consumption of HFD induced whole-body glucose intolerance, and within muscle attenuated insulin-induced Akt phosphorylation, mitochondrial ADP sensitivity (higher apparent K
Identifiants
pubmed: 35398714
pii: S2213-2317(22)00079-9
doi: 10.1016/j.redox.2022.102307
pmc: PMC9006675
pii:
doi:
Substances chimiques
Insulin
0
Nitrates
0
Adenosine Diphosphate
61D2G4IYVH
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
AMP-Activated Protein Kinases
EC 2.7.11.31
Sirt1 protein, mouse
EC 3.5.1.-
Sirtuin 1
EC 3.5.1.-
Glucose
IY9XDZ35W2
Lysine
K3Z4F929H6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
102307Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.