4.2 Article

Gender-specific expression of multiple estrogen receptors, growth hormone receptors, insulin-like growth factors and vitellogenins, and effects of 17β-estradiol in the male tilapia (Oreochromis mossambicus)

Journal

GENERAL AND COMPARATIVE ENDOCRINOLOGY
Volume 156, Issue 3, Pages 544-551

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygcen.2008.03.002

Keywords

insulin-like growth factor; vitellogenin; estrogen receptor; growth hormone receptor; 17 beta-estradiol; growth; reproduction; tilapia

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Gender-specific expression of estrogen receptors (ER alpha and ER beta), growth hormone receptors (GHR1 and GHR2), insulin-like growth factors (IGF-I and IGF-II) and three vitellogenins (Vgs A-C) was examined in the liver, gonad, pituitary, and brain of sexually mature male, female, and 17 beta-estradiol (E-2)-treated male tilapia (Oreochromis mossambicus). Reflecting greater growth rate in male tilapia, hepatic expression of GHR1, GHR2, IGF-I and IGF-II as well as plasma IGF-I levels were higher in males than in females, whereas the expression of Vgs A-C and ER alpha was higher in females. On the other hand, expression of all genes measured was higher in the ovary than in testis. Forty eight hours after E-2 injection (5 mu g/g) into male fish, hepatic expression of most transcripts measured were altered to levels that were similar to those seen in females. The changes included decreased expression of GHR1, GHR2, IGF-I, and IGF-II, and increased expression of ER alpha and Vgs A-C. E-2 treatment also increased Vg and decreased IGF-I in the plasma. Brain expression of ER alpha, ER beta, GHR1, and IGF-I was higher in females than in males, whereas pituitary expression of GHR2 and IGF-I was lower in females; only brain expression of GHR1 was increased by E-2 treatment. These findings suggest that E-2 stimulates Vg production primarily through activation of ER alpha and down-regulation of the GH/IGF-I axis, thus shifting energy from somatic growth towards vitellogenesis at the level of the liver. (c) 2008 Elsevier Inc. All rights reserved.

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