- MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
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Hui Ran, Yao Lu, Qi Zhang, Qiuyue Hu, Junmei Zhao, Kai Wang, Xuemei Tong, Qing Su
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Diabetes Metab J. 2021;45(5):797-797. Published online September 30, 2021
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DOI: https://doi.org/10.4093/dmj.2021.0251
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Corrects: Diabetes Metab J 2021;45(3):439
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- Basic Research
- MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
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Hui Ran, Yao Lu, Qi Zhang, Qiuyue Hu, Junmei Zhao, Kai Wang, Xuemei Tong, Qing Su
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Diabetes Metab J. 2021;45(3):439-451. Published online May 18, 2020
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DOI: https://doi.org/10.4093/dmj.2019.0212
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Correction in: Diabetes Metab J 2021;45(5):797
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7,422
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197
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Abstract
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Background
Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.
Methods
We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.
Results
MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.
Conclusion
MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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Citations
Citations to this article as recorded by
- The Function of MondoA and ChREBP Nutrient—Sensing Factors in Metabolic Disease
Byungyong Ahn International Journal of Molecular Sciences.2023; 24(10): 8811. CrossRef - Normal and Neoplastic Growth Suppression by the Extended Myc Network
Edward V. Prochownik, Huabo Wang Cells.2022; 11(4): 747. CrossRef - The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity
Huiyi Ke, Yu Luan, Siming Wu, Yemin Zhu, Xuemei Tong Frontiers in Endocrinology.2021;[Epub] CrossRef
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