Neuromedin S is a newly identified 36-amino acid peptide in the rat brain, named 'S' after its specific expression in the Suprachiasmatic nucleus. EMBO J. 2005 Jan 26;24(2):325-35. with small amounts in the testis and spleen.
Previously Neuromedin U had been shown to be an anorexigenic hormone with suppressive effects on fasting-induced feeding in rats when administered intracerebroventricularly. Nature. 2000 Jul 6;406(6791):70-4. Neuromedin U gene disruption (as in Neuromedin KO mice) results in obesity. Nat Med. 2004 Oct;10(10):1067-73. Neuromedin S seems to be the endogenous ligand for Neuromedin U type1 and type 2 receptors. This affinity of the Neuromedin U receptors for Neuromedin S made it likely that Neuromedin S may have anorexigenic actions as well. Intracerebroventricular injection of Neuromedin S in rats produces a reduction in food intake over a 12 hour period. Neuromedin S blocks the orexigenic effects of NPY, Ghrelin and AgRP. Endocrinology. 2005 Jun 23; This antagonism seems to be mediated by increasing the POMC and CRH mRNA levels in the PVN, as shown by a blockade of this effect by pre-treatment with antagonist to alpha MSH or CRH. This is in contrast to Neuromedin U which seems to produce its actions mainly through an increase in CRH rather than MSH, as shown by a lack of effect of Neuromedin U in CRH knock out mice. Biochem Biophys Res Commun. 2003 Nov 28;311(4):954-8. This difference in downstream mechanisms of feeding regulation by Neuromedin S and U is intriguing despite common receptors. A difference in intrinsic rhythmic expression in the suprachiasmatic nucleus has been proposed to explain this variation. Biochem Biophys Res Commun. 2004 May 21;318(1):156-61. The possibility of Neuromedin S being a downstream signal for Leptin rather than an independently acting signal Nat Med. 2004 Oct;10(10):1067-73. is being investigated now that specific antisera are becoming available to distinguish Neuromedin U and S.
Previously Neuromedin U had been shown to be an anorexigenic hormone with suppressive effects on fasting-induced feeding in rats when administered intracerebroventricularly. Nature. 2000 Jul 6;406(6791):70-4. Neuromedin U gene disruption (as in Neuromedin KO mice) results in obesity. Nat Med. 2004 Oct;10(10):1067-73. Neuromedin S seems to be the endogenous ligand for Neuromedin U type1 and type 2 receptors. This affinity of the Neuromedin U receptors for Neuromedin S made it likely that Neuromedin S may have anorexigenic actions as well. Intracerebroventricular injection of Neuromedin S in rats produces a reduction in food intake over a 12 hour period. Neuromedin S blocks the orexigenic effects of NPY, Ghrelin and AgRP. Endocrinology. 2005 Jun 23; This antagonism seems to be mediated by increasing the POMC and CRH mRNA levels in the PVN, as shown by a blockade of this effect by pre-treatment with antagonist to alpha MSH or CRH. This is in contrast to Neuromedin U which seems to produce its actions mainly through an increase in CRH rather than MSH, as shown by a lack of effect of Neuromedin U in CRH knock out mice. Biochem Biophys Res Commun. 2003 Nov 28;311(4):954-8. This difference in downstream mechanisms of feeding regulation by Neuromedin S and U is intriguing despite common receptors. A difference in intrinsic rhythmic expression in the suprachiasmatic nucleus has been proposed to explain this variation. Biochem Biophys Res Commun. 2004 May 21;318(1):156-61. The possibility of Neuromedin S being a downstream signal for Leptin rather than an independently acting signal Nat Med. 2004 Oct;10(10):1067-73. is being investigated now that specific antisera are becoming available to distinguish Neuromedin U and S.