Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 8, 1999
Publication Date: N/A
Interpretive Summary: It is well documented that growth hormone administration to red meat animals, in particular swine, consistently improves growth performance including average daily gain and feed efficiency, with marked changes in the composition of gain characterized by enhanced muscle growth and reduced fat tissue deposition. In general, exogenous growth hormone administration has failed to improve growth, and in particular, skeletal muscle deposition in domestic poultry. This study was conducted to further explore why broiler chickens do not respond to growth hormone in a manner similar to mammals. It was determined that all mechanisms are functional in birds, except that growth hormone, unlike the situation in pigs, induces secondary metabolic changes, which negates any positive response to growth hormone. These secondary changes involve the thyroid gland and the metabolism of its products. This information will be of interest to both poultry producers and other scientists.
Despite well documented anabolic effects of GH in mammals, a clear demonstration of such responses in domestic poultry is lacking. Recently, dose-response studies of GH action in the chicken have been conducted using recombinant GH administered to female broilers. GH reduced feed intake (FI) and body weight gain in a dose-dependent manner. The reduction in voluntary Y protein and mRNA were reduced. Growth of breast muscle was also reduced. Muscle free 3-methylhistidine content was not changed, suggesting that a depression in protein synthesis rather than increased degradation occurred. Neither circulating nor breast muscle IGF-I were enhanced by GH, despite evidence that early events in the GH signalling pathway were intact, including binding of GH t its receptor (GHR), association of JAK2 with the GH/GHR complex, and dose-dependent enhancement of JAK2 protein and increase in circulating T3 concentrations, with a maximal increase, paralleled decreases in hepatic 5D-III monodeiodinase activity, whereas 5'D-I activity was not altered. This confirms that a marked hyperthyroid response to GH occurs in late posthatch chickens, resulting from a decrease in the degradative pathway of T3 metabolism. This secondary hyperthyroidism would account for the decreased skeletal muscle mass and lack of enhanced tissue IGF-I in GH treated birds. It is now evident that GH does in fact have important effects in poultry, but that secondary metabolic responses confound the anabolic potential of the hormone.