Abstract
11-ketotestosterone (11-KT) has previously been shown to promote previtellogenic ovarian development and vitellogenin-related hepatic responses in sterlet (Acipenser ruthenus), but the endocrine genes involved in this process remain unclear. In this study, previtellogenic female sterlets were implanted with slow-release 11-KT strips at 5 or 25 mg/kg for 30 days, and transcriptional responses of HPG-axis-related genes, including GnRH paralogs, gonadotropins, and gonadotropin receptors, were examined in the brain-pituitary complex, liver, and ovary. In the brain-pituitary complex, 11-KT increased fsh expression in the 25 mg/kg group and upregulated fshr in both treatment groups, whereas gnrh paralogs showed limited responses. In the liver, most GnRH- and gonadotropin-related genes were not significantly altered, suggesting that hepatic expression of upstream reproductive-axis genes was not a major in vivo target of 11-KT feedback. The ovary exhibited the strongest response, with increased gnrh2 and fsh expression and reduced gnrh3, fshr, and lhr expression, especially at the higher dose. To further examine receptor-related regulation of hepatic vtg expression, liver tissue was incubated in vitro with 11-KT alone or in combination with the androgen receptor antagonist flutamide or the estrogen receptor antagonist fulvestrant. Flutamide did not abolish 11-KT-induced vtg expression, whereas high-dose fulvestrant reduced both era and vtg expression relative to 11-KT treatment alone. Overall, 11-KT elicited tissue-specific transcriptional responses in HPG-axis-related genes, particularly involving ovarian gnrh2, fsh, fshr, and lhr. The differential antagonist responses observed in liver explants provide in vitro evidence consistent with the involvement of ER-associated signaling in hepatic vtg expression, but do not establish direct receptor-mediated regulation.