The organ systems involved in energy homeostasis work in synergy to achieve the maintenance of whole body energy balance. As the largest metabolically active tissue in the body, skeletal muscle is a key determinant of resting energy expenditure and therefore plays a vital role in maintaining energy balance. Communication with other organs, including adipose tissue, is achieved through the secretion of molecular messengers into the circulation, termed myokines. Myostatin, a member of the transforming growth factor b family of secreted growth factors, is one such myokine. The initial studies showed that mice lacking the myostatin gene were kinase inhibitors extremely hypermuscular and had minimal body fat when compared to their wild-type counterparts. To date, myostatin has been widely characterised as a potent negative regulator of skeletal muscle mass and methods to inhibit myostatin function as a potential therapeutic treatment for increasing muscle mass in diseases such as muscular dystrophy and cancer cachexia have been explored. Myostatin is synthesised as an inactive precursor protein which subsequently undergoes two cleavages to produce the mature, active form of the protein. Mature myostatin is bound noncovalently to its propeptide and circulates in serum as an inactive complex. Active, mature myostatin binds selectively to the activin type II receptor kinase, ActRIIB. Studies in rodents and humans generally report that myostatin expression levels are highest in skeletal muscle, although it has also been identified in adipose tissue. Previous work from this laboratory supports these findings and extends them to the horse. These data confirmed that myostatin gene and precursor protein expression is greatest in skeletal muscles and that in the horse, although low levels of expression were detected in adipose tissue at the gene level, myostatin precursor protein was absent. Work in murine models and humans has identified that myostatin may have an important role in obesity development. Myostatin knock-out mice offered high-fat diets are resistant to gains in body fat, and although this effect may be secondary to the increases in lean body mass, myostatin had direct effects on adipocyte differentiation. Furthermore, blocking myostatin increased the functional capacity of brown adipose tissue and may even drive the browning of white adipose tissue through the up-regulation of BAT-specific genes. Myostatin gene expression was positively associated with obesity in both mouse and human studies, whilst blocking myostatin function in mature mice elicited positive effects on glucose and insulin dynamics. In comparison to human and rodent studies, there are fewer studies of myostatin in horses and ponies, and the extant reports generally focus on the identification of a number of single nucleotide polymorphisms in the myostatin gene. SNPs have been associated with different attributes including breeds of different morphological type, optimal race distance in Thoroughbred horses and skeletal muscle fibre type proportions in Quarter horses. To date, no work has been conducted to characterize the expression myostatin and its receptor against the setting of obesity in the horse or pony.