Korean J Obes.  2011 Sep;20(3):91-98.

Myostatin as a Potential Therapeutic Target for Obesity and Insulin Resistance

• Jeong KH
• Choi CS

Abstract

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 beta (TGFbeta) family member, and is known to act as a negative regulator of skeletal muscle differentiation and growth. Like other TGFbeta 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.

Keyword

Myostatin; Muscle growth; Obesity; Insulin resistance

MeSH Terms

Animals
Cell Membrane
Glucose
Humans
Hyperplasia
Hypertrophy
Insulin
Insulin Resistance
Mice
Muscle, Skeletal
Muscles
Myostatin
Obesity
Phosphotransferases
Signal Transduction
Transforming Growth Factor beta
Glucose
Insulin
Myostatin
Phosphotransferases
Transforming Growth Factor beta