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Gonzalez-Franquesa, A.* ; Gama-Perez, P.* ; Kulis, M.* ; Szczepanowska, K.* ; Dahdah, N.* ; Moreno-Gomez, S.* ; Latorre-Pellicer, A.* ; Fernández-Ruiz, R.* ; Aguilar-Mogas, A.* ; Hoffmann, A. ; Monelli, E.* ; Samino, S.* ; Miró-Blanch, J.* ; Oemer, G.* ; Duran, X.* ; Sanchez-Rebordelo, E.* ; Schneeberger, M.* ; Obach, M.* ; Montane, J.* ; Castellano, G.* ; Chapaprieta, V.* ; Sun, W.* ; Navarro, L.* ; Prieto, I.* ; Castaño, C.* ; Novials, A.* ; Gomis, R.* ; Monsalve, M.* ; Claret, M.* ; Graupera, M.* ; Soria, G.* ; Wolfrum, C.* ; Vendrell, J.* ; Fernández-Veledo, S.* ; Enríquez, J.A.* ; Carracedo, A.* ; Perales, J.C.* ; Nogueiras, R.* ; Herrero, L.* ; Trifunovic, A.* ; Keller, M.A.* ; Yanes, O.* ; Sales-Pardo, M.* ; Guimerà, R.* ; Blüher, M. ; Martín-Subero, J.I.* ; Garcia-Roves, P.M.*

Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue.

Redox Biol. 54:102353 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Caloric Restriction ; Exercise ; Human Obesity ; Metabolic Fingerprint ; Metabolic Plasticity ; Mitochondrial Dysfunction ; Multi-organ Approach ; Obesity ; Two-steps Bariatric Surgery ; Visceral Adipose Tissue
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2213-2317
e-ISSN 2213-2317
Zeitschrift Redox Biology
Quellenangaben Band: 54, Heft: , Seiten: , Artikelnummer: 102353 Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
DOI 10.1016/j.redox.2022.102353
WOS ID WOS:000861768000002
Scopus ID 85133597848
PubMed ID 35777200
Erfassungsdatum 2022-11-02
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