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Hormonal regulation of hepatic IGF‐I and IGF‐II gene expression in the Marine Teleost Sparus aurata

Identifieur interne : 000937 ( Main/Exploration ); précédent : 000936; suivant : 000938

Hormonal regulation of hepatic IGF‐I and IGF‐II gene expression in the Marine Teleost Sparus aurata

Auteurs : Oliana Carnevali [Italie] ; Marco Cardinali [Italie] ; Francesca Maradonna [Italie] ; Marco Parisi [Italie] ; Ike Olivotto [Italie] ; Alberta M. Polzonetti-Magni [Italie] ; Gilberto Mosconi [Italie] ; Bruria Funkenstein [Israël]

Source :

RBID : ISTEX:90C23EE996802E47ABC8B6A9211037321268A2D8

English descriptors

Abstract

The present work aimed to determine whether GnRH potentiates the effect of growth hormone (GH) on insulin‐like growth factors (IGF‐I and IGF‐II) hepatic gene expression in Sparus aurata liver. Since several hepatic genes were shown to underlie direct regulation via the hepatic estrogen receptor, another aim was to extend our understanding of direct estrogen effects on liver IGFs gene expression. Pre‐reproductive sea bream females were treated with GH, GnRH, estradiol‐17β, GH plus GnRH, and estradiol‐17β plus GH. After 72 hr, all treatment induced an increase of plasma estradiol well correlated with the increase of plasma vitellogenin (VTG) levels. IGF‐I and IGF‐II expression in the liver of treated females was determined by semi‐quantitative RT‐PCR, using beta‐actin as internal standard. The results reported here show that GH significantly stimulates hepatic transcription of IGF‐I and IGF‐II genes. Surprisingly, E2 and GnRH treatments decreased both IGF‐I and IGF‐II mRNA levels. In fishes treated with GH plus GnRH, the GnRH contrasted the GH effect: the IGF‐I mRNA levels were still significantly higher than in controls, while the effect of GH on IGF‐II gene expression was totally abolished. At the same time, in the combined treatment with GH plus E2, the E2 counteracted the stimulatory effect of GH on both IGF‐I and IGF‐II genes expression. Mol. Reprod. Dev. 71: 12–18, 2005. © 2005 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/mrd.20122


Affiliations:


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