ONTOGENIC STUDY OF INSULIN-LIKE GROWTH-FACTOR-I AND GROWTH-HORMONE RECEPTOR MESSENGER-RNA EXPRESSION IN PORCINE LIVER AND SKELETAL-MUSCLE

The growth hormone-insulin-like growth factor (GH-IGF) axis is involve d in the control of postnatal growth in all animals studied to date. A t 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 tire changes in serum IGF-1 and IGF-2 and GHR mRNA in liver and skeletal mu scle 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 mRN A expressed was found to be predominantly class 1 transcripts with ver y few class 2 transcripts. There was a plateau of liver IGF-1 mRNA lev els after 20 days and up to 140 days, even though the expression of GH R mRNA continued to increase. The levels of expression of the two gene s 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 expr ession of both genes in the LD muscle were highly valuable, with no ag e related changes being observed. However, a significant negative con elation of expression of the two genes was observed (R = -0.60, P < 0. 001), with the correlation still being significant in the two age peri ods. The data are consistent with a likely initial dependence for post natal growth upon GH-stimulated IGF-1 mRNA expression by the liver, up to 20 days of age. After this time, hepatic expression of lGF-1 mRNA reaches a plateau, even though the serum IGF-1 and hepatic GHR mRNA le vels continue to rise. A possible explanation for this could (b)e an i ncrease in either turn-over or stability of IGF-1 mRNA, giving vise to increased levels of peptide with no apparent change in mRNA level. An other possibility is that an increased expression/production of the IG F-binding proteins leads to an increase in the half-life of the peptid e in the circulation.