Abstract

The effects of chicken growth hormone (cGH) infusion on insulin-like growth factor (IGF-I) gene expression in rapidly-growing, meat-type chickens was investigated. Chicken GH was infused either continuously or in a pulsatile fashion to 8-week-old birds during a 7-day period. Following cGH infusion, both IFG-I peptide and IGF-I mRNA content were measured in selected tissues. Steady-state IGF-I mRNA abundance was determined by a solution hybridization nuclease protection assay using total cellular RNA obtained from liver, heart, kidney, spleen, epiphyseal growth plate cartilage, gastrocnemius and pectoralis muscles. Continuous infusion of cGH elicited a two-fold increase in IGF-I peptide concentration in the kidney ( P < 0.05), while all other tissues remained unchanged by cGH treatment under this infusion pattern. Pulsatile cGH infusion produced a two-fold increase in IGF-I peptide content in the liver, gastrocnemius, and pectoralis muscles ( P < 0.05). In contrast with the levels of IGI-I peptide, relative steady-state IGF-I mRNA content was two-fold higher in liver and spleen of birds treated continuously with cGH, but was decreased to 35 and 55% of control birds in heart and pectoralis muscle. Pulsatile cGH infusion resulted in a 64% increase in IGF-I mRNA in the liver and remained unchanged in other tissues. Under both patterns of administration, changes in IGF-I mRNA were not reflected by changes in tissue IGF-I peptide levels. Overall correlations between tissue IGF-I mRNA and peptide levels were low and not significant in the tissues studied, except for liver under pulsatile infusion, in which IGF-I peptide levels paralleled changes in IGF-I mRNA. We conclude that, in chickens, exogenous cGH treatment stimulates hepatic IGF-I transcription and translation only when the pattern of infusion mimics the natural episodic pattern of GH secretion. The low correlation between IGF-I peptide and mRNA levels in extra-hepatic tissues may indicate differential responsiveness to GH in birds, and that in some tissues IGF-I levels are under GH-independent transcriptional controls.

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