Articles producció científica> Medicina i Cirurgia

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

  • Dades identificatives

    Identificador: imarina:9271529
    Autors:
    Gonzalez-Franquesa, AlbaGama-Perez, PauKulis, MartaSzczepanowska, KarolinaDahdah, NormaMoreno-Gomez, SoniaLatorre-Pellicer, AnaFernandez-Ruiz, RebecaAguilar-Mogas, AntoniHoffman, AnneMonelli, ErikaSamino, SaraMiro-Blanch, JoanOemer, GregorDuran, XavierSanchez-Rebordelo, EstrellaSchneeberger, MarcObach, MerceMontane, JoelCastellano, GiancarloChapaprieta, VicenteSun, WenfeiNavarro, LourdesPrieto, IgnacioCastano, CarlosNovials, AnnaGomis, RamonMonsalve, MariaClaret, MarcGraupera, MarionaSoria, GuadalupeWolfrum, ChristianVendrell, JoanFernandez-Veledo, SoniaAntonio Enriquez, JoseCarracedo, AngelCarlos Perales, JoseNogueiras, RubenHerrero, LauraTrifunovic, AleksandraKeller, Markus AYanes, OscarSales-Pardo, MartaGuimera, RogerBlueher, MatthiasIgnacio Martin-Subero, JoseGarcia-Roves, Pablo M
    Resum:
    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.
  • Altres:

    Autor segons l'article: Gonzalez-Franquesa, Alba; Gama-Perez, Pau; Kulis, Marta; Szczepanowska, Karolina; Dahdah, Norma; Moreno-Gomez, Sonia; Latorre-Pellicer, Ana; Fernandez-Ruiz, Rebeca; Aguilar-Mogas, Antoni; Hoffman, Anne; Monelli, Erika; Samino, Sara; Miro-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; Castano, Carlos; Novials, Anna; Gomis, Ramon; Monsalve, Maria; Claret, Marc; Graupera, Mariona; Soria, Guadalupe; Wolfrum, Christian; Vendrell, Joan; Fernandez-Veledo, Sonia; Antonio Enriquez, Jose; Carracedo, Angel; Carlos Perales, Jose; Nogueiras, Ruben; Herrero, Laura; Trifunovic, Aleksandra; Keller, Markus A; Yanes, Oscar; Sales-Pardo, Marta; Guimera, Roger; Blueher, Matthias; Ignacio Martin-Subero, Jose; Garcia-Roves, Pablo M
    Departament: Enginyeria Química Enginyeria Electrònica, Elèctrica i Automàtica Medicina i Cirurgia
    Autor/s de la URV: Fernandez Veledo, Sonia / Guimera Manrique, Roger / Miró Blanch, Joan / Sales Pardo, Marta / SAMINO GENÉ, SARA / Vendrell Ortega, Juan José / Yanes Torrado, Óscar
    Paraules clau: Visceral adipose tissue Two-steps bariatric surgery Oxidative stress Obesity Multi-organ approach Mitochondrial dysfunction Metabolic plasticity Metabolic fingerprint Human obesity Exercise Caloric restriction visceral adipose tissue two-steps bariatric surgery proteomics multi-organ approach mitochondrial dysfunction mice metabolism metabolic plasticity metabolic fingerprint links inflammation increases human obesity gene-expression exercise dysfunction diet caloric restriction
    Resum: 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.
    Àrees temàtiques: Química Organic chemistry Odontología Medicina ii Medicina i Farmacia Clinical biochemistry Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Biotecnología Biodiversidade Biochemistry & molecular biology Biochemistry Astronomia / física
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    Adreça de correu electrònic de l'autor: roger.guimera@urv.cat oscar.yanes@urv.cat sonia.fernandez@urv.cat joan.miro@estudiants.urv.cat juanjose.vendrell@urv.cat marta.sales@urv.cat
    Identificador de l'autor: 0000-0002-3597-4310 0000-0003-3695-7157 0000-0003-2906-3788 0000-0003-3179-0554 0000-0002-6994-6115 0000-0002-8140-6525
    Data d'alta del registre: 2024-10-12
    Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
    Enllaç font original: https://www.sciencedirect.com/science/article/pii/S2213231722001252
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referència a l'article segons font original: Redox Biology. 54 102353-
    Referència de l'ítem segons les normes APA: Gonzalez-Franquesa, Alba; Gama-Perez, Pau; Kulis, Marta; Szczepanowska, Karolina; Dahdah, Norma; Moreno-Gomez, Sonia; Latorre-Pellicer, Ana; Fernandez (2022). Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue. Redox Biology, 54(), 102353-. DOI: 10.1016/j.redox.2022.102353
    DOI de l'article: 10.1016/j.redox.2022.102353
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2022
    Tipus de publicació: Journal Publications
  • Paraules clau:

    Biochemistry,Biochemistry & Molecular Biology,Clinical Biochemistry,Organic Chemistry
    Visceral adipose tissue
    Two-steps bariatric surgery
    Oxidative stress
    Obesity
    Multi-organ approach
    Mitochondrial dysfunction
    Metabolic plasticity
    Metabolic fingerprint
    Human obesity
    Exercise
    Caloric restriction
    visceral adipose tissue
    two-steps bariatric surgery
    proteomics
    multi-organ approach
    mitochondrial dysfunction
    mice
    metabolism
    metabolic plasticity
    metabolic fingerprint
    links
    inflammation
    increases
    human obesity
    gene-expression
    exercise
    dysfunction
    diet
    caloric restriction
    Química
    Organic chemistry
    Odontología
    Medicina ii
    Medicina i
    Farmacia
    Clinical biochemistry
    Ciências biológicas iii
    Ciências biológicas ii
    Ciências biológicas i
    Biotecnología
    Biodiversidade
    Biochemistry & molecular biology
    Biochemistry
    Astronomia / física
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