Ghrelin Stimulates Growth Hormone And Prolactin Release In The Tilapia, Oreochromis Mossambicus

Abstract

Ghrelin (Ghr) is a gut-brain peptide with potent growth hormone (GH)-releasing and orexigenic activities. Ghrelin is synthesized mainly in the oxintic mucosal cells of the stomach, but is expressed to varying degrees in many other tissues, thus suggesting both endocrine and paracrine functions. Ghrelin is the endogenous ligand of the growth hormone secretagogue (GHS) receptor. The characterization of ghrelin's actions has demonstrated that the control of growth hormone cell function and growth is more complex than previously thought. Recently, two forms of ghrelin, ghrelin-C8 and -C 10, were identified in the tilapia, Oreochromis mossambicus. The present study describes in vitro and in vivo effects of the endogenous ghrelins on the release of GH, prolactin (PRL), and insulin-like growth factor-I (IGF-I) in the tilapia. Ghrelin-C8 (100 nM) stimulated GH release in vitro from primary culture of cells prepared from proximal pars distalis containing GH cells and also from whole pituitary after 4 and 8 h. Both forms of ghrelin (100 nM) stimulated GH release from organ-cultured pituitaries after 4 and 8 h, although effect of ghrelin-C8 was not significant at 4h. Lower doses of ghrelin-Cl0 (0.1 and 1 nM) stimulated PRL release from organ-cultured pituitaries after 4 and 8 h. No effect was seen at higher doses (10 and 100 nM). Ghrelin-C8 was without effect on PRL release at any dose. The GHS-receptor-specific antagonist [D-Lys3]-GHRP-6 significantly blocked the stimulatory effect of both forms of ghrelin on GH release from primary cell incubations of pituitary cells. No effect of GHRP-6 was observed on PRL release. Intraperitoneal injection of ghrelin-CI0 at 1ng/g body weight elevated plasma GH levels 5 and 10 h. Plasma levels of IGF-I were also increased by both forms of ghrelin (1 ng/g) after 10 h following injection, whereas no effect was seen on plasma PRL. These results indicate that ghrelin is involved in regulation of GH release through GHS receptor, although it is still possible that ghrelin stimulates 1GF-I release acting directly on hepatocytes.