A role for di-acetyl α-melanocyte-stimulating hormone in the control of cortisol release in the teleost Oreochromis mossambicus

Abstract

ABSTRACT In stressed tilapia, Oreochromis mossambicus, total α-melanocyte-stimulating hormone (α-MSH) levels and di-acetyl α-MSH/mono-acetyl α-MSH (di:mono) ratios are elevated. We therefore investigated the role of α-MSH in the regulation of the pituitary–interrenal axis. The corticotrophic activities of des-acetyl α-MSH, mono-acetyl α-MSH and di-acetyl α-MSH were compared. These forms of α-MSH were isolated from neurointermediate lobes and tested in a superfusion experiment with homologous interrenal tissue. The corticotrophic activity of di-acetyl α-MSH was the highest, followed by that of des-acetyl α-MSH and mono-acetyl α-MSH. Apparently, acetylation of α-MSH is of functional significance for corticotrophic action. Di-acetyl α-MSH proved to be about 100 times less potent than ACTH(1–39): the half-maximal stimulating concentrations for ACTH and di-acetyl α-MSH were 0·89 nmol/l and 110 nmol/l respectively. Surprisingly, a superfusate from neurointermediate lobes proved to be only about three times less active than a superfusate from the pituitary pars distalis, in which the corticotrophic activity is attributable to its ACTH content. When selectively stripped of all forms of α-MSH by passage through a Sepharose column coated with an antiserum against α-MSH the neurointermediate lobe superfusate was devoid of corticotrophic activity. Thus α-MSH appears to be the corticotrophic factor in the superfusate of the neurointermediate lobe. After the same treatment, the corticotrophic activity of the pars distalis superfusate was not affected. We conclude that (in vivo) an as yet unidentified factor is co-released with α-MSH from the neurointermediate lobe, and that this potentiates its corticotrophic activity. Journal of Endocrinology (1992) 135, 285–292