Published in

Cambridge University Press, British Journal of Nutrition, 3(94), p. 353-361, 2005

DOI: 10.1079/bjn20051521

Links

Tools

Export citation

Search in Google Scholar

Regulation of the somatotropic axis by dietary factors in rainbow trout (Oncorhynchus mykiss)

This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Green circle
Preprint: archiving allowed
Orange circle
Postprint: archiving restricted
Red circle
Published version: archiving forbidden
Data provided by SHERPA/RoMEO

Abstract

The activity of the somatotropic axis was analysed in juvenile rainbow trout (Oncorhynchus mykiss) fed either a fishmeal-based diet (FM) or graded levels of plant proteins to replace 50 % (PP50 diet), 75 % (PP75 diet) or 100 % (PP100 diet) of the fishmeal protein. For this purpose, partial cloning and sequencing of the gene encoding rainbow trout growth hormone receptor (GHR) was first accomplished by RT-PCR, using degenerate primers based on the sequences of non-salmonid fish GHR. Growth rates and energy retention were lowered by the PP75 and PP100 diets and a concurrent and progressive increase in plasma levels of growth hormone (GH) was found. However, no changes in hepatic GH binding and total plasma insulin-like growth factor (IGF)-I levels were observed among the four experimental groups. This fact agrees with the lack of changes in hepatic measurements of GHR and IGF-I transcripts. No consistent changes in IGF transcripts were found in peri-visceral adipose tissue and skeletal muscle, but GHR mRNA was up-regulated in the peri-visceral adipose tissue of fish fed the PP75 and PP100 diets, which would favour the lipolytic action of GH. Two specific bands (47 and 33 kDa) of IGF-binding proteins were found in the plasma of all analysed fish, but the sum of the two integrated areas increased progressively with plant protein supply, which might reflect a reduced free IGF availability. Therefore, in our experimental model, the growth impairment could be due, at least in part, to a lowered availability of biologically active IGF (free IGF fraction) rather than to liver GH desensitization or defect in IGF synthesis and release at the systemic and/or paracrine–autocrine level.