GH-Thyroid axis interactions--consequences for muscle growth
In contrast to most vertebrates, GH reportedly has no effect upon somatic growth of the chicken (c). However, previous studies employed only 1-2 dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated effects of 0, 10, 50, 100 and 200 mg/kg BW/d cGH (0-200GH) infused i.v. for 7 days in a pulsatile pattern to immature, growing broiler chickens (9-10 birds/dosage). Comprehensive profiles of thyroid hormone metabolism and measures of somatic growth were obtained.
Overall (average) body weight gain was reduced 25% by GH, with a curvilinear, dose-dependent decrease in skeletal (breast) muscle mass that was maximal (12%) at 100GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (DIII) activity and increases in plasma T3, with both also maximal (74 and 108%, respectively) at 100GH. No effect on type I deiodinase was observed. At the maximally effective dosage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold- increases in hepatic IGF-1 protein content, circulating IGF-1 was not altered with GH infusion, suggesting impairment of hepatic IGF-1 release. Significant, GH dose-dependent increases in plasma NEFA and glucose, and overall decreases in triacylglycerides were also observed. At 200GH, feed intake (FI) was significantly reduced (19%; P<0.05) versus controls, however, additional control birds pair-fed to this level did not exhibit any responses observed for GH birds.
The results of this study support a pathway by which GH impacts on thyroid hormone metabolism beginning at a pretranslational level, with reduced hepatic 5DIII gene expression, translating to reduced protein (enzyme) expression, and reflected in a reduced level of peripheral T3-degrading activity. This contributes to decreased conversion of T3 to its inactive form, thereby elevating circulating T3 levels. The hyper-T3 state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-1.
In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF-1-mediated skeletal muscle growth.