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Hormonal regulation of hepatic IGF‐I and IGF‐II gene expression in the Marine Teleost Sparus aurata
Author(s) -
Carnevali Oliana,
Cardinali Marco,
Maradonna Francesca,
Parisi Marco,
Olivotto Ike,
PolzonettiMagni Alberta M.,
Mosconi Gilberto,
Funkenstein Bruria
Publication year - 2005
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20122
Subject(s) - biology , endocrinology , medicine , vitellogenin , estrogen , gene expression , messenger rna , hormone , insulin like growth factor , receptor , gene , growth factor , biochemistry
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, E 2 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 E 2 , the E 2 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.