Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue
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Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue. / Gonzalez-Franquesa, Alba; Gama-Perez, Pau; Kulis, Marta; Szczepanowska, Karolina; Dahdah, Norma; Moreno-Gomez, Sonia; Latorre-Pellicer, Ana; Fernández-Ruiz, Rebeca; Aguilar-Mogas, Antoni; Hoffman, Anne; Monelli, Erika; Samino, Sara; Miró-Blanch, Joan; Oemer, Gregor; Duran, Xavier; Sanchez-Rebordelo, Estrella; Schneeberger, Marc; Obach, Merce; Montane, Joel; Castellano, Giancarlo; Chapaprieta, Vicente; Sun, Wenfei; Navarro, Lourdes; Prieto, Ignacio; Castaño, Carlos; Novials, Anna; Gomis, Ramon; Monsalve, Maria; Claret, Marc; Graupera, Mariona; Soria, Guadalupe; Wolfrum, Christian; Vendrell, Joan; Fernández-Veledo, Sonia; Enríquez, Jose Antonio; Carracedo, Angel; Perales, José Carlos; Nogueiras, Rubén; Herrero, Laura; Trifunovic, Aleksandra; Keller, Markus A.; Yanes, Oscar; Sales-Pardo, Marta; Guimerà, Roger; Blüher, Matthias; Martín-Subero, José Ignacio; Garcia-Roves, Pablo M.
In: Redox Biology, Vol. 54, 102353, 2022.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue
AU - Gonzalez-Franquesa, Alba
AU - Gama-Perez, Pau
AU - Kulis, Marta
AU - Szczepanowska, Karolina
AU - Dahdah, Norma
AU - Moreno-Gomez, Sonia
AU - Latorre-Pellicer, Ana
AU - Fernández-Ruiz, Rebeca
AU - Aguilar-Mogas, Antoni
AU - Hoffman, Anne
AU - Monelli, Erika
AU - Samino, Sara
AU - Miró-Blanch, Joan
AU - Oemer, Gregor
AU - Duran, Xavier
AU - Sanchez-Rebordelo, Estrella
AU - Schneeberger, Marc
AU - Obach, Merce
AU - Montane, Joel
AU - Castellano, Giancarlo
AU - Chapaprieta, Vicente
AU - Sun, Wenfei
AU - Navarro, Lourdes
AU - Prieto, Ignacio
AU - Castaño, Carlos
AU - Novials, Anna
AU - Gomis, Ramon
AU - Monsalve, Maria
AU - Claret, Marc
AU - Graupera, Mariona
AU - Soria, Guadalupe
AU - Wolfrum, Christian
AU - Vendrell, Joan
AU - Fernández-Veledo, Sonia
AU - Enríquez, Jose Antonio
AU - Carracedo, Angel
AU - Perales, José Carlos
AU - Nogueiras, Rubén
AU - Herrero, Laura
AU - Trifunovic, Aleksandra
AU - Keller, Markus A.
AU - Yanes, Oscar
AU - Sales-Pardo, Marta
AU - Guimerà, Roger
AU - Blüher, Matthias
AU - Martín-Subero, José Ignacio
AU - Garcia-Roves, Pablo M.
N1 - Publisher Copyright: © 2022 The Author(s)
PY - 2022
Y1 - 2022
N2 - 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.
AB - 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.
KW - Caloric restriction
KW - Exercise
KW - Human obesity
KW - Metabolic fingerprint
KW - Metabolic plasticity
KW - Mitochondrial dysfunction
KW - Multi-organ approach
KW - Obesity
KW - Two-steps bariatric surgery
KW - Visceral adipose tissue
U2 - 10.1016/j.redox.2022.102353
DO - 10.1016/j.redox.2022.102353
M3 - Journal article
C2 - 35777200
AN - SCOPUS:85133597848
VL - 54
JO - Redox Biology
JF - Redox Biology
SN - 2213-2317
M1 - 102353
ER -
ID: 314440782