NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle

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NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle. / Henriquez-Olguin, Carlos; Meneses-Valdes, Roberto; Raun, Steffen H.; Gallero, Samantha; Knudsen, Jonas R.; Li, Zhencheng; Li, Jingwen; Sylow, Lykke; Jaimovich, Enrique; Jensen, Thomas E.

In: Redox Biology, Vol. 65, 102842, 2023.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Henriquez-Olguin, C, Meneses-Valdes, R, Raun, SH, Gallero, S, Knudsen, JR, Li, Z, Li, J, Sylow, L, Jaimovich, E & Jensen, TE 2023, 'NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle', Redox Biology, vol. 65, 102842. https://doi.org/10.1016/j.redox.2023.102842

APA

Henriquez-Olguin, C., Meneses-Valdes, R., Raun, S. H., Gallero, S., Knudsen, J. R., Li, Z., Li, J., Sylow, L., Jaimovich, E., & Jensen, T. E. (2023). NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle. Redox Biology, 65, [102842]. https://doi.org/10.1016/j.redox.2023.102842

Vancouver

Henriquez-Olguin C, Meneses-Valdes R, Raun SH, Gallero S, Knudsen JR, Li Z et al. NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle. Redox Biology. 2023;65. 102842. https://doi.org/10.1016/j.redox.2023.102842

Author

Henriquez-Olguin, Carlos ; Meneses-Valdes, Roberto ; Raun, Steffen H. ; Gallero, Samantha ; Knudsen, Jonas R. ; Li, Zhencheng ; Li, Jingwen ; Sylow, Lykke ; Jaimovich, Enrique ; Jensen, Thomas E. / NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle. In: Redox Biology. 2023 ; Vol. 65.

Bibtex

@article{62f3347bc95942da96dd84c5ae47e5ec,
title = "NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle",
abstract = "The production of reactive oxygen species (ROS) by NADPH oxidase (NOX) 2 has been linked to both insulin resistance and exercise training adaptations in skeletal muscle. This study explores the previously unexamined role of NOX2 in the interplay between diet-induced insulin resistance and exercise training (ET). Using a mouse model that harbors a point mutation in the essential NOX2 regulatory subunit, p47phox (Ncf1*), we investigated the impact of this mutation on various metabolic adaptations. Wild-type (WT) and Ncf1* mice were assigned to three groups: chow diet, 60% energy fat diet (HFD), and HFD with access to running wheels (HFD + E). After a 16-week intervention, a comprehensive phenotypic assessment was performed, including body composition, glucose tolerance, energy intake, muscle insulin signaling, redox-related proteins, and mitochondrial adaptations. The results revealed that NOX2 deficiency exacerbated the impact of HFD on body weight, body composition, and glucose intolerance. Moreover, in Ncf1* mice, ET did not improve glucose tolerance or increase muscle cross-sectional area. ET normalized body fat independently of genotype. The lack of NOX2 activity during ET reduced several metabolic adaptations in skeletal muscle, including insulin signaling and expression of Hexokinase II and oxidative phosphorylation complexes. In conclusion, these findings suggest that NOX2 mediates key beneficial effects of exercise training in the context of diet-induced obesity.",
keywords = "Faculty of Science, Exercise, Metabolism, Insulin sensitivity",
author = "Carlos Henriquez-Olguin and Roberto Meneses-Valdes and Raun, {Steffen H.} and Samantha Gallero and Knudsen, {Jonas R.} and Zhencheng Li and Jingwen Li and Lykke Sylow and Enrique Jaimovich and Jensen, {Thomas E.}",
note = "Publisher Copyright: {\textcopyright} 2023 The Authors",
year = "2023",
doi = "10.1016/j.redox.2023.102842",
language = "English",
volume = "65",
journal = "Redox Biology",
issn = "2213-2317",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle

AU - Henriquez-Olguin, Carlos

AU - Meneses-Valdes, Roberto

AU - Raun, Steffen H.

AU - Gallero, Samantha

AU - Knudsen, Jonas R.

AU - Li, Zhencheng

AU - Li, Jingwen

AU - Sylow, Lykke

AU - Jaimovich, Enrique

AU - Jensen, Thomas E.

N1 - Publisher Copyright: © 2023 The Authors

PY - 2023

Y1 - 2023

N2 - The production of reactive oxygen species (ROS) by NADPH oxidase (NOX) 2 has been linked to both insulin resistance and exercise training adaptations in skeletal muscle. This study explores the previously unexamined role of NOX2 in the interplay between diet-induced insulin resistance and exercise training (ET). Using a mouse model that harbors a point mutation in the essential NOX2 regulatory subunit, p47phox (Ncf1*), we investigated the impact of this mutation on various metabolic adaptations. Wild-type (WT) and Ncf1* mice were assigned to three groups: chow diet, 60% energy fat diet (HFD), and HFD with access to running wheels (HFD + E). After a 16-week intervention, a comprehensive phenotypic assessment was performed, including body composition, glucose tolerance, energy intake, muscle insulin signaling, redox-related proteins, and mitochondrial adaptations. The results revealed that NOX2 deficiency exacerbated the impact of HFD on body weight, body composition, and glucose intolerance. Moreover, in Ncf1* mice, ET did not improve glucose tolerance or increase muscle cross-sectional area. ET normalized body fat independently of genotype. The lack of NOX2 activity during ET reduced several metabolic adaptations in skeletal muscle, including insulin signaling and expression of Hexokinase II and oxidative phosphorylation complexes. In conclusion, these findings suggest that NOX2 mediates key beneficial effects of exercise training in the context of diet-induced obesity.

AB - The production of reactive oxygen species (ROS) by NADPH oxidase (NOX) 2 has been linked to both insulin resistance and exercise training adaptations in skeletal muscle. This study explores the previously unexamined role of NOX2 in the interplay between diet-induced insulin resistance and exercise training (ET). Using a mouse model that harbors a point mutation in the essential NOX2 regulatory subunit, p47phox (Ncf1*), we investigated the impact of this mutation on various metabolic adaptations. Wild-type (WT) and Ncf1* mice were assigned to three groups: chow diet, 60% energy fat diet (HFD), and HFD with access to running wheels (HFD + E). After a 16-week intervention, a comprehensive phenotypic assessment was performed, including body composition, glucose tolerance, energy intake, muscle insulin signaling, redox-related proteins, and mitochondrial adaptations. The results revealed that NOX2 deficiency exacerbated the impact of HFD on body weight, body composition, and glucose intolerance. Moreover, in Ncf1* mice, ET did not improve glucose tolerance or increase muscle cross-sectional area. ET normalized body fat independently of genotype. The lack of NOX2 activity during ET reduced several metabolic adaptations in skeletal muscle, including insulin signaling and expression of Hexokinase II and oxidative phosphorylation complexes. In conclusion, these findings suggest that NOX2 mediates key beneficial effects of exercise training in the context of diet-induced obesity.

KW - Faculty of Science

KW - Exercise

KW - Metabolism

KW - Insulin sensitivity

U2 - 10.1016/j.redox.2023.102842

DO - 10.1016/j.redox.2023.102842

M3 - Journal article

C2 - 37572454

VL - 65

JO - Redox Biology

JF - Redox Biology

SN - 2213-2317

M1 - 102842

ER -

ID: 362142324