Effects of Selective Myostatin Inhibitor PAH-A on Broiler Skeletal Muscle Production

Abstract

A fivefold increase in worldwide meat production over the past 50 years has fueled research in muscle physiology toward the development of methods to increase skeletal muscle growth in agricultural animals. A breakthrough in the exploration of muscle production occurred in 1997 with the identification of myostatin, a negative regulator for skeletal muscle development. Mutations in the myostatin gene have been shown to increase skeletal muscle growth in several species including mice, cattle, and humans. A natural mutation in this gene results in the double muscling phenotype of Belgian Blue cattle (Figure 1). Some strategies proven to repress myostatin function, such as the administration of myostatin-specific antibodies or the use of a soluble activin type II receptor (ActRIIBFc), reduce the binding affinity of myostatin to its receptor, activin receptor type II B (ActRIIB). Pfizer Animal Health Compound A (PAH-A), a selective myostatin inhibitor, also impedes the attachment of myostatin to ActRIIB. The effectiveness of PAH-A in augmenting skeletal muscle growth has not previously been described in poultry. The ultimate goal of our study was to investigate the effects of PAH-A on skeletal muscle production in broilers. We hypothesized that in ovo administration of PAH-A would increase body mass gain (BMG) and muscle fiber cross-sectional-area (CSA) of standard broilers at post-hatch days 3 (D3) and 14 (D14).