SAT-LB069 Differential Regulation of Hypothalamic and Hepatic Reproductive Signals by Leptin and Sex Steroids in the Mozambique Tilapia Oreochromis mossambicus

Reproduction is a physiologically demanding process that relies on energy sufficiency, the lack of which can result in delayed puberty and suppression of reproductive function. The pleiotropic peptide hormone leptin is a key signal in energy homeostasis that relays information on peripheral energy availability to central circuits. In mammals, leptin has been found to serve as a critical permissive signal in the activation of the gonadotropic axis and onset of puberty. Although leptin effects on reproduction have been explored extensively in mammals, its actions and regulatory properties on reproduction in fishes remain unclear. The current study assesses (i) the effect of in vivo leptin treatment on hypothalamic kisspeptin (kiss2) and gonadotropin-releasing hormone (gnrh1), (ii) the effect of leptin treatment on major egg-yolk precursors, vitellogenins (vtga, vtgb, vtgc), and insulin-like growth factor (igf1) in primary tilapia hepatocytes, and (iii) the effect of sex steroid treatment on leptin (lep) and insulin-like growth factor in primary tilapia hepatocytes. Gene expression of lep in the liver, the primary source of circulating hormone, increased with gonadosomatic index and sexual maturation of male and female tilapia, suggesting the hormone may regulate reproductive function. Intraperitoneal injection and 6-hour treatment with recombinant tilapia leptin (rtLep) in adult male tilapia resulted in increased hypothalamic kiss2 and gnrh1 transcript levels versus saline control (P < 0.01). In primary hepatocyte culture, rtLep suppressed vtgb and vtgc transcript levels (P < 0.01), while it stimulated igf1 (P < 0.0001). Testosterone and estradiol reduced lep levels (P < 0.001), but disparately regulated ­igf1 whereby testosterone increased igf1 and estradiol decreased igf1 at 10 and 100 nM (P < 0.001). The non-aromatizable 11-ketotestosterone increased lep and igf1 transcript levels at 100 nM (P < 0.05). Our findings suggest that leptin expression rises with sexual maturation and the hormone exerts stimulatory effects on hypothalamic gonadotropic factors. By contrast, leptin reduces estrogen-sensitive vitellogenesis while promoting elements of the somatotropic axis (e.g., igf1), suggesting the hormone may have dual roles in regulating reproductive and somatic growth processes. We speculate that this latter effect may be associated with limiting energy partitioning to reproduction in instances of negative energy balance. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.