Kits
Myostatin ELISA
Kits
Description
Myostatin belongs to the transforming growth differentiation factor-ß (TGF-ß) super
family. The molecule is a negative regulator of muscle growth, but details about the
actions of myostatin are uncertain (Roth and Walsh, 2004).
Myostatin was first identified in 1997 by McPherron et al. They found out that nullmutant
knockout mice were significantly larger than wild-type animals and exhibited
a large and widespread increase in skeletal muscle mass due to an increase of muscle
fiber number (hyperplasia) and thickness (hypertrophy). Other groups identified mutations
in the myostatin gene in naturally bred “double-muscles” cattle breeds.
Similar to the findings in animal models, increased myostatin immuno-reactivity or
expression has been observed in HIV-infected men with muscle wasting (GonzalesCadavid
et al. 1998), after prolonged bed rest in young men (Zachwieja et al. 1999)
and in older men and women with muscle wasting (Yarasheski KE et al. 2002).
Shi et al. (2007) and others have found that myostatin deficiency inhibits adipogenesis
in vivo, even when mice are fed a high-fat diet. Transgenic overexpression of
myostatin pro-peptide, which inhibits myostatin signaling, also inhibits body fat gain
with a high-fat diet (Zhao et al. 2005). Similar alterations in myostatin signaling are
associated with changes in body fat among humans.
Hittel et al. (2010) report that myostatin-levels are regulated by aerobic exercise.
Moreover, myostatin is in the causal pathway of acquired insulin resistance with
physical inactivity
family. The molecule is a negative regulator of muscle growth, but details about the
actions of myostatin are uncertain (Roth and Walsh, 2004).
Myostatin was first identified in 1997 by McPherron et al. They found out that nullmutant
knockout mice were significantly larger than wild-type animals and exhibited
a large and widespread increase in skeletal muscle mass due to an increase of muscle
fiber number (hyperplasia) and thickness (hypertrophy). Other groups identified mutations
in the myostatin gene in naturally bred “double-muscles” cattle breeds.
Similar to the findings in animal models, increased myostatin immuno-reactivity or
expression has been observed in HIV-infected men with muscle wasting (GonzalesCadavid
et al. 1998), after prolonged bed rest in young men (Zachwieja et al. 1999)
and in older men and women with muscle wasting (Yarasheski KE et al. 2002).
Shi et al. (2007) and others have found that myostatin deficiency inhibits adipogenesis
in vivo, even when mice are fed a high-fat diet. Transgenic overexpression of
myostatin pro-peptide, which inhibits myostatin signaling, also inhibits body fat gain
with a high-fat diet (Zhao et al. 2005). Similar alterations in myostatin signaling are
associated with changes in body fat among humans.
Hittel et al. (2010) report that myostatin-levels are regulated by aerobic exercise.
Moreover, myostatin is in the causal pathway of acquired insulin resistance with
physical inactivity