Participation of AMPK in the Control of Skeletal Muscle Mass
The skeletal muscle plays crucial roles in whole-body glucose, lipid, and energy metabolism and in locomotive functions. The maintenance of the skeletal muscle mass is regulated by protein turnover: the balance between protein synthesis and protein degrad
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Participation of AMPK in the Control of Skeletal Muscle Mass Tatsuro Egawa
Abstract The skeletal muscle plays crucial roles in whole-body glucose, lipid, and energy metabolism and in locomotive functions. The maintenance of the skeletal muscle mass is regulated by protein turnover: the balance between protein synthesis and protein degradation. The metabolic sensor 50 AMP-activated protein kinase (AMPK) has important functions in the maintenance of cellular homeostasis and modulates glucose, lipid, and protein metabolism in the skeletal muscle. Recent studies warrant consideration of AMPK as a crucial regulator of muscle mass and suggest that AMPK controls skeletal muscle hypertrophy and atrophy by suppressing protein synthesis and promoting protein degradation via various signaling pathways. In addition, AMPK may stimulate myogenesis and regeneration of the skeletal muscle from injury. Conversely, the lack of AMPK activation probably restricts protein turnover during aging, potentially contributing to muscle loss. Taken together, these data indicate that AMPK triggers accelerated muscle turnover by regulating protein metabolism and/or myogenesis and thereby facilitates muscle mass homeostasis. Keywords Protein synthesis • Protein degradation • Ubiquitin–proteasome system • Autophagy • Myogenesis
12.1 Introduction The skeletal muscle is the largest tissue in the body, accounting for approximately 40–50% of total body mass and plays crucial roles in whole-body glucose, lipid, and energy metabolism and in locomotive functions. Hence, it is recognized that decreased skeletal muscle function leads to reduced health status and higher
T. Egawa () Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Yoshida-nihonmatsu-cho, Sakyo-ku, Kyoto 606-8501, Japan Department of Physiology, Graduate School of Health Sciences, Toyohashi SOZO University, Toyohashi, Aichi, Japan e-mail: [email protected] © Springer Nature Singapore Pte Ltd. 2017 K. Sakuma (ed.), The Plasticity of Skeletal Muscle, DOI 10.1007/978-981-10-3292-9_12
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mortality. Aging is one of the most important factors that contribute to loss of muscle function and mass. Elderly people lose approximately 1% of muscle mass each year [38] as a natural effect associated with aging. However, muscle mass loss is not unavoidable, warranting the development of strategies for muscle maintenance and studies of the biological mechanisms of muscle mass regulation. Maintenance of muscle mass is regulated by the balance between protein synthesis and protein degradation, which increase and decrease skeletal muscle mass, respectively, with changes in turnover dynamics. Several signaling cascades are associated with this balance and the control of muscle mass. 50 AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that has emerged as a master sensor of cellular energy balance in mammalian cells [45]. AMPK was originally discovered as a kinase associated with critical metabolic
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