Donald Thompson, Brooks, Erica L., Kuliniski, Kristen M.
Somatotropin, also known as growth hormone, is a protein hormone produced and secreted by the pituitary gland of mammals. Somatotropin has several functions in the body, the most notable of which is growth of the long bones (for example, the femur of the thigh), which is achieved via stimulation of an intermediate hormone, insulin-like growth factor-I (IGF-I), from the liver. Failure to produce adequate amounts of somatotropin in young animals results in dwarfism; somatotropin deficiency in adulthood results in muscle weakness and a general feeling of malaise.
Before 1980, the availability of somatotropin for treatment of deficiencies in children or for possible agricultural use was limited to hormone extracted from pituitaries of cadavers (human) or slaughterhouse carcasses. Then, in the early 1980s, scientists developed the technology to produce somatotropin in the laboratory by inserting the somatotropin gene into the DNA of bacteria. Large amounts of somatotropin could be produced by this “recombinant” method, and the technology was quickly adapted for human, cattle and pig somatotropins, all of which differed slightly from one another in amino acid composition. Considerable research followed on the use of bovine somatotropin to increase milk yield in dairy cattle, and Posilac, the first commercially available product for that purpose, came onto the market in 1994.
Recombinant equine somatotropin (eST), produced by an Australian company, was first introduced into the United States for research purposes about the same time Posilac was appearing on the market. Because increasing lactation in broodmares did not seem to be an economically promising use for eST, other possible uses were tested both within the LSU AgCenter (benefits to wound healing and enhancement of ovarian function) and at other universities (Rutgers University: treatment of aged mares; Texas A&M University: treatment for young racehorses in training).
During this time, considerable interest was growing among members of the horse industry in the possible use of eST to enhance the size and performance potential of “stunted” foals, foals born prematurely and even normal foals. Gradually, two schools of thought emerged: 1) that eST was the next “silver bullet” for enhancing horse performance, and 2) that eST was going to lead to the destruction of the horse industry because of its creation of deformed and unhealthy giants.
To clarify the rampant speculation, research was initiated at the LSU AgCenter in 1999 to determine under controlled, scientific conditions whether eST would alter the growth and development patterns of normal, healthy foals. BresaGen, Ltd., the company that produced eST, provided sufficient eST and funds to perform the experiment. Fourteen foals were weaned at 4 to 4.5 months of age and were paired by gender (fillies and geldings) and by body weight and breed type so that the pair mates were as similar as possible.
One foal from each pair was then randomly assigned to be treated with eST (at the recommended dose from the supplier) and the other foal with the vehicle (no eST). They received daily injections in this manner for 12 months. During the experiment, the horses were fed a pelleted grain ration and grass hay so that they received 110 percent of their protein and energy needs determined by the National Research Council and 150 percent of the calcium and phosphorous. These higher nutrient levels were provided based on the large volume of research on pigs at the time, which showed that pigs could not respond appropriately to somatotropin without extra nutrients.
During the 12 months of treatment, the horses were monitored monthly for body weight and various measurements of body size (for example, height at the withers, front cannon bone length). They were also monitored from the hormonal standpoint to determine whether somatotropin treatment altered any other hormonal systems in the body. These hormonal data were also needed for confirming the biological response to the somatotropin.
Results of the experiment provided some useful information for horse breeders. Daily eST treatment did enhance the horses’ blood levels of IGF-I, confirming that the eST was having the expected biological effect. The eST-treated horses did not, however, exhibit any change (positive or negative) in growth rate, body measurements or appearance (for example, muscling). Hormonal analysis indicated that the eST-treated horses had a reduced production of their own pituitary somatotropin and had an exaggerated insulin response to glucose (typical of animals exposed to high somatotropin levels).
This research project provided answers to the two basic questions on eST. No, there was no detectable beneficial effect of eST at the recommended dose on foal growth and development, and no, there were no gross problems, or detrimental side-effects, because of its use. Further research has shown, however, that eST-treated foals do have enlarged internal organs (spleen, kidney, liver), which is not necessarily a desired effect. Thus, it is concluded that eST, although a powerful hormone, does not appear to be a practical means of enhancing the growth of young horses.