Format

Send to

Choose Destination
Gen Comp Endocrinol. 2009 Mar;161(1):79-82. doi: 10.1016/j.ygcen.2008.12.009. Epub 2008 Dec 24.

Seasonal regulation of vitellogenin by growth hormone in the goldfish liver.

Author information

1
Department of Biological Sciences, University of Calgary, 2500 University Drive, N.W., Calgary, Alberta, Canada T2N 1N4.

Abstract

Goldfish, like many other fish species, undergo well-documented annual cycles, which include well-defined somatic and reproductive states. It is known that part of the year is spent in a somatotropic state (usually from late spring to late fall), followed by transition into the reproductive state (usually from late Fall to late Spring). The onset of reproductive cycle is characterized by synthesis of phosphoglycoprotein vitellogenin (Vg), a precursor to the egg yolk proteins in the liver and its uptake in the oocyte. Hormones regulate the process of vitellogenesis and circulating 17-beta-estradiol is known to be a key factor during the reproductive period. During vitellogenesis, pituitary produces growth hormone (GH), but the fish divert most of the energy towards reproduction rather than growth. In this study we investigated the role of GH in the regulation of Vg in goldfish. The goldfish Vg cDNA was partially cloned (1348 amino acids), which included a highly conserved lipoprotein N-terminal domain, and used as a probe for Northern blot analysis. Treatment of female liver in vitro with recombinant goldfish GH increased Vg mRNA in goldfish at early stages of recrudescence (September), but was without effect in mid-late stages of vitellogenesis and post-spawning period (February-June). There was a correlation between GH activity and basal expression levels of the growth hormone receptor (GHR). Like Vg, GHR transcript was increased by treatment with GH in September but not February or June. Overall, the present study provides novel information on the role of GH in the season-dependent regulation of Vg and GHR gene expression.

PMID:
19138687
DOI:
10.1016/j.ygcen.2008.12.009
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center