Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

In contrast to most vertebrates, GH reportedly has no effect upon somatic g rowth of the chicken. However, previous studies employed only one to two do sages of the hormone, and limited evidence exists of a hyperthyroid respons e that may confound its anabolic potential. This study evaluated the effect s of 0, 10, 50, 100 and 200 mug/kg body weight per day chicken GH (cGH) (0- 200 GH) infused i.v. for 7 days in a pulsatile pattern to immature. growing broiler chickens (9-10 birds/dosage). Comprehensive profiles of thyroid ho rmone metabolism and measures of somatic growth were obtained. Overall (average) body weight gain was reduced 25% by GH, with a curvilinea r, dose-dependent decrease in skeletal (breast) muscle mass that was maxima l (12%) at 100 GH. This profile mirrored GH dose-dependent decreases in hep atic type III deiodinase (DIII) activity and increases in plasma tri-iodoth yronine (T-3), with both also maximal (74 and 108% respectively) at 100 GH. No effect on type I deiodinase was observed. At the maximally effective do sage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold-increases in hepatic IGF-I protein content, circulati ng IGF-I was not altered with GH infusion, suggesting impairment of hepatic IGF-I release. Significant, GH dose-dependent increases in plasma non-este rified fatty acid and glucose, and overall decreases in triacylglycerides w ere also observed. At 200 GH, feed intake was significantly reduced (19% P< 0.05) versus controls: however, additional control birds pair-fed to this l evel did not exhibit any responses observed for GH-treated birds. The results of this study support a pathway by which GH impacts on thyroid hormone metabolism beginning at a pretranslational level, with reduced hepa tic DIII gene expression, translating to reduced protein (enzyme) ex pressi on, and reflected in a reduced level of peripheral T-3-degrading activity. This contributes to decreased conversion of T-3 to its inactive form, there by elevating circulating T-3 levels. The hyper-T-3 state leads to reduced n et skeletal muscle deposition, and may impair release of GH-enhanced, hepat ic IGF-I. In conclusion, GH has significant biological effects in the chicken, but pr ofound metabolic actions predominate that may confound positive, IGF-I-medi ated skeletal muscle growth.