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

Alba Gonzalez-Franquesa; Pau Gama-Perez; Marta Kulis; Karolina Szczepanowska; Norma Dahdah; Sonia Moreno-Gomez; Ana Latorre-Pellicer; Rebeca Fernández-Ruiz; Antoni Aguilar-Mogas; Anne Hoffman; Erika Monelli; Sara Samino; Joan Miró-Blanch; Gregor Oemer; Xavier Duran; Estrella Sanchez-Rebordelo; Marc Schneeberger; Merce Obach; Joel Montane; Giancarlo Castellano; Vicente Chapaprieta; Wenfei Sun; Lourdes Navarro; Ignacio Prieto; Carlos Castaño; Anna Novials; Ramon Gomis; Maria Monsalve; Marc Claret; Mariona Graupera; Guadalupe Soria; Christian Wolfrum; Joan Vendrell; Sonia Fernández-Veledo; Jose Antonio Enríquez; Angel Carracedo; José Carlos Perales; Rubén Nogueiras; Laura Herrero; Aleksandra Trifunovic; Markus A. Keller; Oscar Yanes; Marta Sales-Pardo; Roger Guimerà; Matthias Blüher; José Ignacio Martín-Subero; Pablo M. Garcia-Roves

doi:10.1016/j.redox.2022.102353

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

Alba Gonzalez-Franquesa
, Pau Gama-Perez
, Marta Kulis
, Karolina Szczepanowska
, Norma Dahdah
, Sonia Moreno-Gomez
, Ana Latorre-Pellicer
, Rebeca Fernández-Ruiz
, Antoni Aguilar-Mogas
, Anne Hoffman
, Erika Monelli
, Sara Samino
, Joan Miró-Blanch
, Gregor Oemer
, Xavier Duran
, Estrella Sanchez-Rebordelo
, Marc Schneeberger
, Merce Obach
, Joel Montane
, Giancarlo Castellano

Vicente Chapaprieta, Wenfei Sun, Lourdes Navarro, Ignacio Prieto, Carlos Castaño, Anna Novials, Ramon Gomis, Maria Monsalve, Marc Claret, Mariona Graupera, Guadalupe Soria, Christian Wolfrum, Joan Vendrell, Sonia Fernández-Veledo, Jose Antonio Enríquez, Angel Carracedo, José Carlos Perales, Rubén Nogueiras, Laura Herrero, Aleksandra Trifunovic, Markus A. Keller, Oscar Yanes, Marta Sales-Pardo, Roger Guimerà, Matthias Blüher, José Ignacio Martín-Subero, Pablo M. Garcia-Roves^*

^*Corresponding author for this work

Blanquerna School of Health Sciences

Research output: Indexed journal article › Article › peer-review

24 Citations (Scopus)

Abstract

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.

Original language	English
Article number	102353
Journal	Redox Biology
Volume	54
DOIs	https://doi.org/10.1016/j.redox.2022.102353
Publication status	Published - Aug 2022

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Caloric restriction
Exercise
Human obesity
Metabolic fingerprint
Metabolic plasticity
Mitochondrial dysfunction
Multi-organ approach
Obesity
Two-steps bariatric surgery
Visceral adipose tissue

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10.1016/j.redox.2022.102353Licence: CC BY-NC-ND

Cite this

Gonzalez-Franquesa, A., Gama-Perez, P., Kulis, M., Szczepanowska, K., Dahdah, N., Moreno-Gomez, S., Latorre-Pellicer, A., Fernández-Ruiz, R., Aguilar-Mogas, A., Hoffman, A., Monelli, E., Samino, S., Miró-Blanch, J., Oemer, G., Duran, X., Sanchez-Rebordelo, E., Schneeberger, M., Obach, M., Montane, J., ... Garcia-Roves, P. M. (2022). Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue. Redox Biology, 54, Article 102353. https://doi.org/10.1016/j.redox.2022.102353

@article{467e424c85b94f7f8d5259ec299956e7,

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

abstract = "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.",

keywords = "Caloric restriction, Exercise, Human obesity, Metabolic fingerprint, Metabolic plasticity, Mitochondrial dysfunction, Multi-organ approach, Obesity, Two-steps bariatric surgery, Visceral adipose tissue",

author = "Alba Gonzalez-Franquesa and Pau Gama-Perez and Marta Kulis and Karolina Szczepanowska and Norma Dahdah and Sonia Moreno-Gomez and Ana Latorre-Pellicer and Rebeca Fern{\'a}ndez-Ruiz and Antoni Aguilar-Mogas and Anne Hoffman and Erika Monelli and Sara Samino and Joan Mir{\'o}-Blanch and Gregor Oemer and Xavier Duran and Estrella Sanchez-Rebordelo and Marc Schneeberger and Merce Obach and Joel Montane and Giancarlo Castellano and Vicente Chapaprieta and Wenfei Sun and Lourdes Navarro and Ignacio Prieto and Carlos Casta{\~n}o and Anna Novials and Ramon Gomis and Maria Monsalve and Marc Claret and Mariona Graupera and Guadalupe Soria and Christian Wolfrum and Joan Vendrell and Sonia Fern{\'a}ndez-Veledo and Enr{\'i}quez, \{Jose Antonio\} and Angel Carracedo and Perales, \{Jos{\'e} Carlos\} and Rub{\'e}n Nogueiras and Laura Herrero and Aleksandra Trifunovic and Keller, \{Markus A.\} and Oscar Yanes and Marta Sales-Pardo and Roger Guimer{\`a} and Matthias Bl{\"u}her and Mart{\'i}n-Subero, \{Jos{\'e} Ignacio\} and Garcia-Roves, \{Pablo M.\}",

note = "Funding Information: This work has been supported by Ministerio de Ciencia e Innovaci{\'o}n (MICINN) Grant BFU2011- 24679 (P.M.G.-R.); Instituto de Salud Carlos III (ISCIII) Grant PI15/00701 (P.M.G.-R.) cofinanced by the European Regional Development Fund {\textquoteleft}{\textquoteleft}A way to build Europe{\textquoteright}{\textquoteleft}; Government of Catalonia Support Grups de Recerca AGAUR 2017-SGR-204 (to J.C.P. and P.M.G-R.), 2017-SGR-736 (to J.I.M.-S.) and 2017-SGR-896 (to A.A.-M. M.S.-P. and R.G.). M.M. was recipient of a MINECO grant RTI2018-093864-B-I00. O.Y. was funded by MINECO grant BFU2017-87958. M.A.K. was funded by a Medical University of Innsbruck Start Grant. M.C. was funded by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement 725004). L. H. was funded by MINECO grants SAF2013-45887-R, SAF2017-83813-C3-1-R (granted to Dolors Serra (DS) and L.H.), co-funded by the European Regional Development Fund, the Centro de Investigaci{\'o}n Biom{\'e}dica en Red de Fisiopatolog{\'i}a de la Obesidad y la Nutrici{\'o}n (CIBEROBN) (Grant CB06/03/0001 to DS), the Government of Catalonia (2017SGR278 to DS), the Fundaci{\'o} La Marat{\'o} de TV3 (201627–30 to DS), the European Foundation for the Study of Diabetes (EFSD)/Janssen-Rising Star and L'Or{\'e}al-UNESCO “For Women in Science” research fellowships. P.M.G.-R. was a recipient of a Ramon y Cajal contract (RYC-2009-05158) from MICINN. A.G-F. was a recipient of “Beca de Formaci{\'o} de Personal Investigador de l'IDIBAPS” fellowship and she is currently supported by an unconditional donation from the Novo Nordisk Foundation (NNF) to NNF Center for Basic Metabolic Research (NNF18CC0034900). P.G-P. was a recipient of predoctoral fellowship from the Universitat de Barcelona (APIF-UB). K.S was financed through “Advanced Postdoc Grant” from SFB 1218 (DFG, German Reuter Foundation, Projektnummer 269925409). J.M-B. was a recipient of predoctoral fellowship from the European Union's Horizon 2020 research and innovation program under the Marie Sk{\l}odowska-Curie grant agreement 675610. E.S-R. was recipient of a predoctoral fellowship from Ministerio de Economia y Empresa (MINECO) grant BES-2013-062796. This work was partially developed at the Esther Koplowitz Center (CEK, Barcelona, Spain). We want to acknowledge the following experts: Drs. Vidal-Puig A. Malagon M.M. and Raimundo N. for their advice and critical discussion of our work. Funding Information: This work has been supported by Ministerio de Ciencia e Innovaci{\'o}n (MICINN) Grant BFU2011- 24679 (P.M.G.-R.); Instituto de Salud Carlos III (ISCIII) Grant PI15/00701 (P.M.G.-R.) cofinanced by the European Regional Development Fund {\textquoteleft}{\textquoteleft}A way to build Europe{\textquoteright}{\textquoteleft}; Government of Catalonia Support Grups de Recerca AGAUR 2017-SGR-204 (to J.C.P. and P.M.G-R.), 2017-SGR-736 (to J.I.M.-S.) and 2017-SGR-896 (to A.A.-M., M.S.-P., and R.G.). M.M. was recipient of a MINECO grant RTI2018-093864-B-I00. O.Y. was funded by MINECO grant BFU2017-87958 . M.A.K. was funded by a Medical University of Innsbruck Start Grant. M.C. was funded by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement 725004 ). L. H. was funded by MINECO grants SAF2013-45887-R , SAF2017-83813-C3-1-R (granted to Dolors Serra (DS) and L.H.), co-funded by the European Regional Development Fund , the Centro de Investigaci{\'o}n Biom{\'e}dica en Red de Fisiopatolog{\'i}a de la Obesidad y la Nutrici{\'o}n (CIBEROBN) (Grant CB06/03/0001 to DS), the Government of Catalonia ( 2017SGR278 to DS), the Fundaci{\'o} La Marat{\'o} de TV3 ( 201627–30 to DS), the European Foundation for the Study of Diabetes (EFSD)/ Janssen-Rising Star and L{\textquoteright}Or{\'e}al-UNESCO “For Women in Science” research fellowships. P.M.G.-R. was a recipient of a Ramon y Cajal contract ( RYC-2009-05158 ) from MICINN . A.G-F. was a recipient of “ Beca de Formaci{\'o} de Personal Investigador de l'IDIBAPS ” fellowship and she is currently supported by an unconditional donation from the Novo Nordisk Foundation (NNF) to NNF Center for Basic Metabolic Research ( NNF18CC0034900 ). P.G-P. was a recipient of predoctoral fellowship from the Universitat de Barcelona (APIF-UB). K.S was financed through “ Advanced Postdoc Grant ” from SFB 1218 ( DFG, German Reuter Foundation , Projektnummer 269925409 ). J.M-B. was a recipient of predoctoral fellowship from the European Union's Horizon 2020 research and innovation program under the Marie Sk{\l}odowska-Curie grant agreement 675610 . E.S-R. was recipient of a predoctoral fellowship from Ministerio de Economia y Empresa (MINECO) grant BES-2013-062796 . This work was partially developed at the Esther Koplowitz Center (CEK, Barcelona, Spain). We want to acknowledge the following experts: Drs. Vidal-Puig A., Malagon M.M. and Raimundo N. for their advice and critical discussion of our work. Publisher Copyright: {\textcopyright} 2022 The Author(s)",

year = "2022",

month = aug,

doi = "10.1016/j.redox.2022.102353",

language = "English",

volume = "54",

journal = "Redox Biology",

issn = "2213-2317",

publisher = "Elsevier B.V.",

}

Gonzalez-Franquesa, A, Gama-Perez, P, Kulis, M, Szczepanowska, K, Dahdah, N, Moreno-Gomez, S, Latorre-Pellicer, A, Fernández-Ruiz, R, Aguilar-Mogas, A, Hoffman, 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, JA, Carracedo, A, Perales, JC, Nogueiras, R, Herrero, L, Trifunovic, A, Keller, MA, Yanes, O, Sales-Pardo, M, Guimerà, R, Blüher, M, Martín-Subero, JI & Garcia-Roves, PM 2022, 'Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue', Redox Biology, vol. 54, 102353. https://doi.org/10.1016/j.redox.2022.102353

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 - Funding Information: This work has been supported by Ministerio de Ciencia e Innovación (MICINN) Grant BFU2011- 24679 (P.M.G.-R.); Instituto de Salud Carlos III (ISCIII) Grant PI15/00701 (P.M.G.-R.) cofinanced by the European Regional Development Fund ‘‘A way to build Europe’‘; Government of Catalonia Support Grups de Recerca AGAUR 2017-SGR-204 (to J.C.P. and P.M.G-R.), 2017-SGR-736 (to J.I.M.-S.) and 2017-SGR-896 (to A.A.-M. M.S.-P. and R.G.). M.M. was recipient of a MINECO grant RTI2018-093864-B-I00. O.Y. was funded by MINECO grant BFU2017-87958. M.A.K. was funded by a Medical University of Innsbruck Start Grant. M.C. was funded by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement 725004). L. H. was funded by MINECO grants SAF2013-45887-R, SAF2017-83813-C3-1-R (granted to Dolors Serra (DS) and L.H.), co-funded by the European Regional Development Fund, the Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y la Nutrición (CIBEROBN) (Grant CB06/03/0001 to DS), the Government of Catalonia (2017SGR278 to DS), the Fundació La Marató de TV3 (201627–30 to DS), the European Foundation for the Study of Diabetes (EFSD)/Janssen-Rising Star and L'Oréal-UNESCO “For Women in Science” research fellowships. P.M.G.-R. was a recipient of a Ramon y Cajal contract (RYC-2009-05158) from MICINN. A.G-F. was a recipient of “Beca de Formació de Personal Investigador de l'IDIBAPS” fellowship and she is currently supported by an unconditional donation from the Novo Nordisk Foundation (NNF) to NNF Center for Basic Metabolic Research (NNF18CC0034900). P.G-P. was a recipient of predoctoral fellowship from the Universitat de Barcelona (APIF-UB). K.S was financed through “Advanced Postdoc Grant” from SFB 1218 (DFG, German Reuter Foundation, Projektnummer 269925409). J.M-B. was a recipient of predoctoral fellowship from the European Union's Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement 675610. E.S-R. was recipient of a predoctoral fellowship from Ministerio de Economia y Empresa (MINECO) grant BES-2013-062796. This work was partially developed at the Esther Koplowitz Center (CEK, Barcelona, Spain). We want to acknowledge the following experts: Drs. Vidal-Puig A. Malagon M.M. and Raimundo N. for their advice and critical discussion of our work. Funding Information: This work has been supported by Ministerio de Ciencia e Innovación (MICINN) Grant BFU2011- 24679 (P.M.G.-R.); Instituto de Salud Carlos III (ISCIII) Grant PI15/00701 (P.M.G.-R.) cofinanced by the European Regional Development Fund ‘‘A way to build Europe’‘; Government of Catalonia Support Grups de Recerca AGAUR 2017-SGR-204 (to J.C.P. and P.M.G-R.), 2017-SGR-736 (to J.I.M.-S.) and 2017-SGR-896 (to A.A.-M., M.S.-P., and R.G.). M.M. was recipient of a MINECO grant RTI2018-093864-B-I00. O.Y. was funded by MINECO grant BFU2017-87958 . M.A.K. was funded by a Medical University of Innsbruck Start Grant. M.C. was funded by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement 725004 ). L. H. was funded by MINECO grants SAF2013-45887-R , SAF2017-83813-C3-1-R (granted to Dolors Serra (DS) and L.H.), co-funded by the European Regional Development Fund , the Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y la Nutrición (CIBEROBN) (Grant CB06/03/0001 to DS), the Government of Catalonia ( 2017SGR278 to DS), the Fundació La Marató de TV3 ( 201627–30 to DS), the European Foundation for the Study of Diabetes (EFSD)/ Janssen-Rising Star and L’Oréal-UNESCO “For Women in Science” research fellowships. P.M.G.-R. was a recipient of a Ramon y Cajal contract ( RYC-2009-05158 ) from MICINN . A.G-F. was a recipient of “ Beca de Formació de Personal Investigador de l'IDIBAPS ” fellowship and she is currently supported by an unconditional donation from the Novo Nordisk Foundation (NNF) to NNF Center for Basic Metabolic Research ( NNF18CC0034900 ). P.G-P. was a recipient of predoctoral fellowship from the Universitat de Barcelona (APIF-UB). K.S was financed through “ Advanced Postdoc Grant ” from SFB 1218 ( DFG, German Reuter Foundation , Projektnummer 269925409 ). J.M-B. was a recipient of predoctoral fellowship from the European Union's Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement 675610 . E.S-R. was recipient of a predoctoral fellowship from Ministerio de Economia y Empresa (MINECO) grant BES-2013-062796 . This work was partially developed at the Esther Koplowitz Center (CEK, Barcelona, Spain). We want to acknowledge the following experts: Drs. Vidal-Puig A., Malagon M.M. and Raimundo N. for their advice and critical discussion of our work. Publisher Copyright: © 2022 The Author(s)

PY - 2022/8

Y1 - 2022/8

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

UR - https://www.scopus.com/pages/publications/85133597848

UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=pure_univeritat_ramon_llull&SrcAuth=WosAPI&KeyUT=WOS:000861768000002&DestLinkType=FullRecord&DestApp=WOS_CPL

UR - http://hdl.handle.net/20.500.14342/3984

U2 - 10.1016/j.redox.2022.102353

DO - 10.1016/j.redox.2022.102353

M3 - Article

C2 - 35777200

AN - SCOPUS:85133597848

SN - 2213-2317

VL - 54

JO - Redox Biology

JF - Redox Biology

M1 - 102353

ER -

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

Abstract

UN SDGs

Keywords

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