Mitochondrial Redox Status Regulates Glycogen Metabolism via Glycogen Phosphorylase Activity

Mitochondria and glycogen are co-distributed in skeletal muscles to regulate the metabolic status. Mitochondria are also redox centers that regulate the muscle function during exercise. However, the pathophysiological relationship between the mitochondrial redox status and glycogen metabolism in the...

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Bibliographic Details
Published in:Antioxidants 2024-11, Vol.13 (11), p.1421
Main Authors: Sakamoto, Ikko, Shibuya, Shuichi, Nojiri, Hidetoshi, Takeno, Kotaro, Nishimune, Hiroshi, Yaku, Keisuke, Nakagawa, Takashi, Ishijima, Muneaki, Shimizu, Takahiko
Format: Article
Language:English
Subjects:
Aging
Antioxidants
Chemical industry
Disease
Enzymes
Ethylenediaminetetraacetic acid
Exercise
Fitness equipment
Glucose
Glucose metabolism
Glycogen
Glycogen phosphorylase
Metabolism
Mitochondria
Muscle fatigue
Muscle function
Muscles
Musculoskeletal system
Mutants
Neomycin
Paraquat
Phosphorylase
Physical fitness
redox balance
Respiration
Running
Skeletal muscle
SOD2
Superoxide
Superoxide dismutase
Synthesis
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Summary:Mitochondria and glycogen are co-distributed in skeletal muscles to regulate the metabolic status. Mitochondria are also redox centers that regulate the muscle function during exercise. However, the pathophysiological relationship between the mitochondrial redox status and glycogen metabolism in the muscle remains unclear. In the present study, we examined the pathological effects of mitochondrial dysfunction induced by mitochondrial superoxide dismutase (SOD2) depletion on glycogen metabolism. We found that muscle glycogen was significantly accumulated in association with motor dysfunction in mice with a muscle-specific SOD2 deficiency. Muscle glycogen phosphorylase (GP-M) activity, which is a key enzyme for glycogen degradation at times when energy is needed (e.g., during exercise), was significantly decreased in the mutant muscle. Moreover, the GP-M activity on normal muscle sections decreased after treatment with paraquat, a superoxide generator. In contrast, treatment with antioxidants reversed the GP-M activity and motor disturbance of the mutant mice, indicating that GP-M activity was reversibly regulated by the redox balance. These results demonstrate that the maintenance of the mitochondrial redox balance regulates glycogen metabolism via GP-M activity.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox13111421