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KMID : 0388120110200030091
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Journal of Korean Society for the Study of Obesity
2011 Volume.20 No. 3 p.91 ~ p.98
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Myostatin as a Potential Therapeutic Target for Obesity and Insulin Resistance
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Jeong Kyeong-Hoon
Choi Cheol-Soo
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Abstract
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Considering that skeletal muscle is a major tissue responsible for whole body glucose and fat disposal, it has long been speculated that increasing muscle mass would be a potential therapeutic strategy to prevent obesity and fat-induced insulin resistance. Myostatin (growth differentiation factor 8, GDF8) is a transforming growth factor β (TGFβ) family member, and is known to act as a negative regulator of skeletal muscle differentiation and growth. Like other TGFβ members, dimeric myostatin mediates Sma/Mothers against decapentaplegic homolog (SMAD) signal transduction through its specific cell membrane receptors with serine/threonine kinase activity. Myostatin null (Mstn-/-) mice exhibit a doubling of muscle mass due to muscle hypertrophy and hyperplasia, and are protected against fat-induced obesity and insulin resistance. Other genetic and pharmacologic approaches to inhibit myostatin activity also demonstrate an increase in muscle mass and a prevention of obesity and insulin resistance. This review will focus on the effects of myostatin inhibition on obesity and fat-induced insulin resistance, and will discuss the potential underlying mechanisms.
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KEYWORD
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Myostatin, Muscle growth, Obesity, Insulin resistance
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