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

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-...

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Autores: González Franquesa, Alba, Gama-Perez, Pau, Kulis, Marta, Szczepanowska, K., Dahdah, Norma, Moreno-Gomez, Sonia, Latorre Pellicer, Ana, Fernández Ruiz, Rebeca, Aguilar-Mogas, Antoni, Hoffman, Anne, Monelli, Erika, Samino Gené, 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, 1946-, Monsalve, Maria, Claret i Carles, Marc, Graupera i Garcia-Milà, Mariona, Soria, Guadalupe, Wolfrum, Christian, Vendrell, Joan, Fernández-Veledo, Sonia, Enriquez, Jose Antonio, Carracedo Álvarez, Ángel, Perales Losa, 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.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/190251
Acceso en línea:https://hdl.handle.net/2445/190251
Access Level:acceso abierto
Palabra clave:Resistència a la insulina
Obesitat
Teixit adipós
Mitocondris
Insulin resistance
Obesity
Adipose tissues
Mitochondria
Descripción
Sumario: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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