Ontogenic study of insulin-like growth factor-1 and growth hormone receptor mRNA expression in porcine liver and skeletal muscle

Abstract

AbstractThe growth hormone-insulin-like growth factor (GH-IGF) axis is involved in the control of postnatal growth in all animals studied to date. At birth, blood levels of IGF-1 are low, although levels of GH are high. Thus a switching occurs during the postnatal period, which involves an increase in liver GH-receptors (GHR). This study investigates the changes in serum IGF-1 and IGF-1 and GHR mRNA in liver and skeletal muscle of growing pigs. The period from birth to 20 days of age showed a gradual increase in both IGF-1 and GHR mRNA expression by the liver, thus accounting for the gradual increase in serum IGF-1. The IGF-1 mRNA expressed was found to be predominantly class 1 transcripts with very few class 2 transcripts. There was a plateau of liver IGF-1 mRNA levels after 20 days and up to 140 days, even though the expression of GHR mRNA continued to increase. The levels of expression of the two genes were found to correlate in the first 20-day period (r = 0·76,P< 0·005), but not in the later period (r = 0·44,P> 0·05).Levels of expression of both genes in the LD muscle were highly variable, with no age related changes being observed. However, a significant negative correlation of expression of the two genes was observed (R = 0·60,P< 0·001), with the correlation still being significant in the two age periods.The data are consistent with a likely initial dependence for postnatal growth upon GH-stimulated IGF-1 mRNA expression by the liver, up to 20 days of age. After this time, hepatic expression of IGF-1 mRNA reaches a plateau, even though the serum IGF-1 and hepatic GHR mRNA levels continue to rise. A possible explanation for this could be an increase in either turn-over or stability of IGF-1 mRNA, giving rise to increased levels of peptide with no apparent change in mRNA level. Another possibility is that an increased expression/production of the IGF-binding proteins leads to an increase in the half-life of the peptide in the circulation.