Adipocyte-specific Nos2 deletion improves insulin resistance and dyslipidemia through brown fat activation in diet-induced obese mice.
Dyslipidemia
Insulin resistance
Mitochondrial respiration
Nitric oxide synthase
Obesity
brown adipose tissue
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
03 2022
03 2022
Historique:
received:
20
05
2021
revised:
22
12
2021
accepted:
03
01
2022
pubmed:
17
1
2022
medline:
5
4
2022
entrez:
16
1
2022
Statut:
ppublish
Résumé
Inducible nitric oxide (NO) synthase (NOS2) is a well-documented inflammatory mediator of insulin resistance in obesity. NOS2 expression is induced in both adipocytes and macrophages within adipose tissue during high-fat (HF)-induced obesity. Eight-week-old male mice with adipocyte selective deletion of the Nos2 gene (Nos2 HFHS-fed Nos2 These results demonstrate the key role of adipocyte NOS2 in the development of obesity-linked insulin resistance and dyslipidemia, partly through NO-dependent inhibition of BAT mitochondrial bioenergetics.
Identifiants
pubmed: 35033724
pii: S2212-8778(22)00006-0
doi: 10.1016/j.molmet.2022.101437
pmc: PMC8802131
pii:
doi:
Substances chimiques
Nitric Oxide Synthase Type II
EC 1.14.13.39
Nos2 protein, mouse
EC 1.14.13.39
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101437Subventions
Organisme : CIHR
ID : FDN 143247
Pays : Canada
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier GmbH.. All rights reserved.