| Type |
Article |
| Date |
2005-09 |
| Language |
English |
| Author(s) |
Gomez Requeni P2, Calduch Giner J2, de Celis S2, Medale Francoise1, 3, Kaushik Sadasivam1, 3, Perez Sanchez Jaume3 |
| Affiliation(s) |
1 : IFREMER, Unite Mixte INRA, Lab Nutr Poissons, F-64310 St Pee Sur Nivelle, France.
2 : CSIC, Inst Acuicultura Torre Sal, Castellon, Spain. |
| Source |
British Journal of Nutrition (0007-1145) (Cambridge University Press), 2005-09 , Vol. 94 , N. 3 , P. 353-361 |
| DOI |
10.1079/BJN20051521 |
| WOS© Times Cited |
45 |
| Keyword(s) |
Insulin like growth factor, Growth hormone receptor, Growth hormone, Plant proteins, Rainbow trout |
| 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. |
| Full Text |
| File |
Pages |
Size |
Access |
| publication-3620.pdf |
9 |
380 KB |
Open access |
|
