Exercise Improves Redox Homeostasis and Mitochondrial Function in White Adipose Tissue.

adipose tissue exercise hormesis redox homeostasis

Journal

Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981

Informations de publication

Date de publication:
29 Aug 2022
Historique:
received: 21 06 2022
revised: 16 08 2022
accepted: 24 08 2022
entrez: 23 9 2022
pubmed: 24 9 2022
medline: 24 9 2022
Statut: epublish

Résumé

Exercise has beneficial effects on energy balance and also improves metabolic health independently of weight loss. Adipose tissue function is a critical denominator of a healthy metabolism but the adaptation of adipocytes in response to exercise is insufficiently well understood. We have previously shown that one aerobic exercise session was associated with increased expression of antioxidant and cytoprotective genes in white adipose tissue (WAT). In the present study, we evaluate the chronic effects of physical exercise on WAT redox homeostasis and mitochondrial function. Adult male Wistar rats were separated into two groups: a control group that did not exercise and a group that performed running exercise sessions on a treadmill for 30 min, 5 days per week for 9 weeks. Reactive oxygen species (ROS) generation, antioxidant enzyme activities, mitochondrial function, markers of oxidative stress and inflammation, and proteins related to DNA damage response were analyzed. In WAT from the exercise group, we found higher mitochondrial respiration in states I, II, and III of Complex I and Complex II, followed by an increase in ATP production, and the ROS/ATP ratio when compared to tissues from control rats. Regarding redox homeostasis, NADPH oxidase activity, protein carbonylation, and lipid peroxidation levels were lower in WAT from the exercise group when compared to control tissues. Moreover, antioxidant enzymatic activity, reduced glutathione/oxidized glutathione ratio, and total nuclear factor erythroid-2, like-2 (NFE2L2/NRF2) protein levels were higher in the exercise group compared to control. Finally, we found that exercise reduced the phosphorylation levels of H2AX histone (γH2AX), a central protein that contributes to genome stability through the signaling of DNA damage. In conclusion, our results show that chronic exercise modulates redox homeostasis in WAT, improving antioxidant capacity, and mitochondrial function. This hormetic remodeling of adipocyte redox balance points to improved adipocyte health and seems to be directly associated with the beneficial effects of exercise.

Identifiants

pubmed: 36139762
pii: antiox11091689
doi: 10.3390/antiox11091689
pmc: PMC9495527
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : European Research Council
ID : PROTEOFIT
Pays : International
Organisme : Coordenação de Aperfeicoamento de Pessoal de Nível Superior
ID : RF
Organisme : National Council for Scientific and Technological Development
ID : RF
Organisme : Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro
ID : RF

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Auteurs

Leonardo Matta (L)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.
Institute for Cardiovascular Prevention, Klinikum der Universität München, Ludwig-Maximilians-University Munich, 80539 München, Germany.
Institute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, 85764 Munich, Germany.

Caroline Coelho de Faria (CC)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Dahienne F De Oliveira (DF)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Iris Soares Andrade (IS)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Niedson Correia Lima-Junior (NC)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Bianca Martins Gregório (BM)

Urogenital Research Unit, Roberto Alcântara Gomes Institute of Biology, State University of Rio de Janeiro, 20511-010 Rio de Janeiro, Brazil.

Cristina Maeda Takiya (CM)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Andrea Claudia Freitas Ferreira (ACF)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.
Multidisciplinary Center for Research in Biology (NUMPEX) Duque de Caxias Campus, Federal University of Rio de Janeiro, 25250-470 Rio de Janeiro, Brazil.

José Hamilton M Nascimento (JHM)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Denise Pires de Carvalho (DP)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Alexander Bartelt (A)

Institute for Cardiovascular Prevention, Klinikum der Universität München, Ludwig-Maximilians-University Munich, 80539 München, Germany.
Institute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, 85764 Munich, Germany.

Leonardo Maciel (L)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.
Multidisciplinary Center for Research in Biology (NUMPEX) Duque de Caxias Campus, Federal University of Rio de Janeiro, 25250-470 Rio de Janeiro, Brazil.

Rodrigo Soares Fortunato (RS)

Health Science Center, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil.

Classifications MeSH