A central component of growth coordination in vertebrates is the growth hormone (GH)-insulin-like growth factor-1 (IGF-1) system. To date, most studies on the control of vertebrate growth have focused on regulation of pituitary GH production and release. In this study, we used liver, muscle, and gill tissue from sexually immature rainbow trout incubated in vitro to evaluate the extrapituitary effects of 17β-estradiol (E2) and testosterone (T) on mRNA and functional expression of growth hormone receptors (GHR), insulin-like growth factors 1 and 2 (IGF-1, IGF-2), and type 1 IGF receptors (IGFR1). E2 significantly decreased steady-state levels of GHR1, GHR2, and IGF-1 mRNAs in liver as well as of GHR1 and GHR2 mRNAs in muscle and of IGF-1 and IGF-2 mRNAs in gill in a time- and concentration-dependent manner. E2 had no effect on levels of IGFR1 mRNAs in muscle or on GHR and IGFR1 mRNAs in gill. Functional expression of GHRs as assessed by 125I-GH binding capacity was reduced by E2 in liver and muscle; however, E2 did not affect 125I-IGF-1 binding capacity in muscle or 125I-GH and 125I-IGF-1 binding capacity in gill. By contrast, T increased steady-state levels of GHR1, GHR2, IGF-1, and IGF-2 mRNAs in liver, of GHR1, GHR2, IGFR1A, and IGFR1B in muscle, and of GHR1, GHR2, IGF-1, IGF-2, IGFR1A, and IGFR1B mRNAs in gill in a time- and concentration-dependent manner. Binding capacity of 125I-GH in liver and of 125I-GH and 125I-IGF-1 in both muscle and gill also was increased by T. These data indicate that E2 and T directly affect peripheral aspects of the GH-IGF system, and suggest, at least in immature rainbow trout, that E2 reduces hepatic sensitivity to GH as well as reduces peripheral production of IGFs and that T increases peripheral sensitivity to GH and IGF as well as increases peripheral production of IGFs.
- Growth hormone receptor
- Growth hormone-insulin-like growth factor system
- Insulin-like growth factor receptor
- Insulin-like growth factor-1
- Insulin-like growth factor-2
- Rainbow trout