Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet
Increase in body fat contributes to loss of function and changes in skeletal muscle, accelerating sarcopenia, a phenomenon known as sarco-obesity or sarcopenic obesity. Studies suggest that obesity decreases the skeletal muscle (SM)’s ability to oxidize glucose, increases fatty acid oxidation and re...
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| Language: | English |
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MDPI AG
2023-03-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/6/5654 |
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| author | Pía Apablaza Juan Carlos Bórquez Rodrigo Mendoza Mónica Silva Gladys Tapia Alejandra Espinosa Rodrigo Troncoso Luis A. Videla Nevenka Juretić Andrea del Campo |
| author_facet | Pía Apablaza Juan Carlos Bórquez Rodrigo Mendoza Mónica Silva Gladys Tapia Alejandra Espinosa Rodrigo Troncoso Luis A. Videla Nevenka Juretić Andrea del Campo |
| author_sort | Pía Apablaza |
| collection | DOAJ |
| description | Increase in body fat contributes to loss of function and changes in skeletal muscle, accelerating sarcopenia, a phenomenon known as sarco-obesity or sarcopenic obesity. Studies suggest that obesity decreases the skeletal muscle (SM)’s ability to oxidize glucose, increases fatty acid oxidation and reactive oxygen species production, due to mitochondrial dysfunction. Exercise improves mitochondrial dysfunction in obesity; however, it is not known if exercise regulates the mitochondrial unfolded protein response (UPRmt) in the SM. Our study aimed to determine the mito-nuclear UPRmt in response to exercise in a model of obesity, and how this response is associated with the improvement in SM functioning after exercise training. C57BL/6 mice were fed a normal diet and high-fat diet (HFD) for 12 weeks. After 8 weeks, animals were subdivided into sedentary and exercised for the remaining 4 weeks. Grip strength and maximal velocity of mice submitted to HFD improved after training. Our results show an increase in the activation of UPRmt after exercise while in obese mice, proteostasis is basally decreased but shows a more pronounced increase with exercise. These results correlate with improvement in the circulating triglycerides, suggesting mitochondrial proteostasis could be protective and could be related to mitochondrial fuel utilization in SM. |
| first_indexed | 2024-03-11T06:25:17Z |
| format | Article |
| id | doaj.art-ac4dca4b10a04067bbf46de908a84f2e |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T06:25:17Z |
| publishDate | 2023-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-ac4dca4b10a04067bbf46de908a84f2e2023-11-17T11:37:06ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-03-01246565410.3390/ijms24065654Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat DietPía Apablaza0Juan Carlos Bórquez1Rodrigo Mendoza2Mónica Silva3Gladys Tapia4Alejandra Espinosa5Rodrigo Troncoso6Luis A. Videla7Nevenka Juretić8Andrea del Campo9Programa de Biología Celular y Molecular, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, ChileLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago 7830490, ChileLaboratorio de Fisiología y Bioenergética Celular, Escuela de Química y Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile, Santiago 7820436, ChileCentro de Estudios de Ejercicio, Metabolismo y Cáncer, Programa de Fisiología y Biofísica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, ChilePrograma de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, ChileEscuela de Medicina, Universidad de Valparaíso, Valparaíso 2340000, ChileLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago 7830490, ChilePrograma de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, ChilePrograma de Biología Celular y Molecular, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, ChileLaboratorio de Fisiología y Bioenergética Celular, Escuela de Química y Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile, Santiago 7820436, ChileIncrease in body fat contributes to loss of function and changes in skeletal muscle, accelerating sarcopenia, a phenomenon known as sarco-obesity or sarcopenic obesity. Studies suggest that obesity decreases the skeletal muscle (SM)’s ability to oxidize glucose, increases fatty acid oxidation and reactive oxygen species production, due to mitochondrial dysfunction. Exercise improves mitochondrial dysfunction in obesity; however, it is not known if exercise regulates the mitochondrial unfolded protein response (UPRmt) in the SM. Our study aimed to determine the mito-nuclear UPRmt in response to exercise in a model of obesity, and how this response is associated with the improvement in SM functioning after exercise training. C57BL/6 mice were fed a normal diet and high-fat diet (HFD) for 12 weeks. After 8 weeks, animals were subdivided into sedentary and exercised for the remaining 4 weeks. Grip strength and maximal velocity of mice submitted to HFD improved after training. Our results show an increase in the activation of UPRmt after exercise while in obese mice, proteostasis is basally decreased but shows a more pronounced increase with exercise. These results correlate with improvement in the circulating triglycerides, suggesting mitochondrial proteostasis could be protective and could be related to mitochondrial fuel utilization in SM.https://www.mdpi.com/1422-0067/24/6/5654obesityUPRmtskeletal muscleexercise |
| spellingShingle | Pía Apablaza Juan Carlos Bórquez Rodrigo Mendoza Mónica Silva Gladys Tapia Alejandra Espinosa Rodrigo Troncoso Luis A. Videla Nevenka Juretić Andrea del Campo Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet International Journal of Molecular Sciences obesity UPRmt skeletal muscle exercise |
| title | Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet |
| title_full | Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet |
| title_fullStr | Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet |
| title_full_unstemmed | Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet |
| title_short | Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet |
| title_sort | exercise induces an augmented skeletal muscle mitochondrial unfolded protein response in a mouse model of obesity produced by a high fat diet |
| topic | obesity UPRmt skeletal muscle exercise |
| url | https://www.mdpi.com/1422-0067/24/6/5654 |
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