Quantification of insulin-like growth factor-1 (IGF-1) mRNA: modulation of growth intensity by feeding results in inter- and intra-tissue-specific differences of IGF-1 mRNA expression in steers.

摘要

The effect of constant and compensating body growth velocities on IGF-1 mRNA expression was studied in various tissues of growing steers. Twenty-six steers were allocated to three groups in which the average daily gains were kept either constantly high on intensive feeding, low on pasture feeding or were accelerated to compensatory growth after feed restriction. All animals were slaughtered at 570+/-2.6 kg and samples were collected from liver, heart, kidney and from 4 different muscles (m. splenius, m. soleus, m. cutaneus truncii and m. semispinalis capitis), which were selected in order to include maximal differences in fibre composition as well as in growth impetus. IGF-1 mRNA was quantified by a validated internally standardised RT-PCR method. The amount of RNA extracted from the various tissues investigated was constant within each type of tissue and showed no differences between treatment groups. As indicated by a constant ratio between the amount of RNA extracted and the DNA concentrations, there was no effect of the feeding on total transcriptional activity. The order of IGF-1 mRNA abundance per g tissue was liver > > kidney > heart > skeletal muscle. The different feeding regimen resulted in significant differences of IGF-1 mRNA expression rates in all organs showing different patterns between organs. IGF-1 mRNA concentrations showed muscle specific differences and also divergent reactions in response to the differing growth rates. These results support that the liver is the main IGF-1 producing tissue; above that they indicate that skeletal muscle, in particular when taking its absolute mass into account, might considerably contribute to the IGF-1 levels in blood. Our findings demonstrate that IGF-1 mRNA expression is regulated tissue specifically not only between different organs but also within musculature.