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

Abstract

In contrast to most vertebrates, GH reportedly has no effect upon somatic growth of the chicken. However, previous studies employed only one to two dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated the effects of 0, 10, 50, 100 and 200 µg/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 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 100 GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (DIII) activity and increases in plasma tri-iodothyronine (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 dosage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold-increases in hepatic IGF-I protein content, circulating IGF-I was not altered with GH infusion, suggesting impairment of hepatic IGF-I release. Significant, GH dose-dependent increases in plasma non-esterified fatty acid and glucose, and overall decreases in triacylglycerides were also observed. At 200 GH, feed intake 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-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 hepatic DIII gene expression, translating to reduced protein (enzyme) expression, and reflected in a reduced level of peripheral T 3 -degrading activity. This contributes to decreased conversion of T 3 to its inactive form, thereby elevating circulating T 3 levels. The hyper-T 3 state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-I.In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF-I-mediated skeletal muscle growth.

Effects of early feed restriction programs on production performance and hormone level in plasma of broiler chickens

“…Vasilatos et al (2000) reported that GH injection decreased the deposition of breast muscle and the leg muscle of broilers, which may be differences of sensitivity of muscle fiber types. Color is one of the main characteristics of meat quality, which is determined by myoglobin content that depends on the myofibril types in muscle.…”

The Hypothalamic-Pituitary-Thyroid (HPT) Axis in Birds and Its Role in Bird Development and Reproduction

“…Together these alterations in deiodination result in the perihatch T 3 peak (see "Deiodination Enzymes" earlier in this article). The effects of GH on 5D III also are present in immature growing broiler chickens (Vasilatos-Younken et al, 2000). Glucocorticoids, which also may influence deiodinases, increase late in incubation/gestation, but in contrast to mammals, they appear not to be an important factor in the changes in deiodination activity at this time in precocial birds (see review in Darras et al, 1995).…”

Evidence of a role for neuropeptide Y and monoamines in mediating the appetite-suppressive effect of GH

“…Plasma concentrations of GH were elevated in a dosedependent fashion with GH infusion, and ranged from 0·3 5·7 ng/ml for controls up to 89·0 5·4 ng/ml at the highest dosage (200 µg/kg BW per day) (for detailed profile see Vasilatos-Younken et al 2000). Plasma GH concentrations for pair-fed groups did not differ from controls (Table 1).…”