Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue.
Caloric restriction
Exercise
Human obesity
Metabolic fingerprint
Metabolic plasticity
Mitochondrial dysfunction
Multi-organ approach
Obesity
Two-steps bariatric surgery
Visceral adipose tissue
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
16
03
2022
revised:
20
05
2022
accepted:
24
05
2022
pubmed:
2
7
2022
medline:
14
7
2022
entrez:
1
7
2022
Statut:
ppublish
Résumé
Metabolic plasticity is the ability of a biological system to adapt its metabolic phenotype to different environmental stressors. We used a whole-body and tissue-specific phenotypic, functional, proteomic, metabolomic and transcriptomic approach to systematically assess metabolic plasticity in diet-induced obese mice after a combined nutritional and exercise intervention. Although most obesity and overnutrition-related pathological features were successfully reverted, we observed a high degree of metabolic dysfunction in visceral white adipose tissue, characterized by abnormal mitochondrial morphology and functionality. Despite two sequential therapeutic interventions and an apparent global healthy phenotype, obesity triggered a cascade of events in visceral adipose tissue progressing from mitochondrial metabolic and proteostatic alterations to widespread cellular stress, which compromises its biosynthetic and recycling capacity. In humans, weight loss after bariatric surgery showed a transcriptional signature in visceral adipose tissue similar to our mouse model of obesity reversion. Overall, our data indicate that obesity prompts a lasting metabolic fingerprint that leads to a progressive breakdown of metabolic plasticity in visceral adipose tissue.
Identifiants
pubmed: 35777200
pii: S2213-2317(22)00125-2
doi: 10.1016/j.redox.2022.102353
pmc: PMC9287736
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
102353Informations de copyright
Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.
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