Cortistatin (CORT), a neuropeptide able to activate GHS-R, has emerged as an additional link in gut-brain interplay. which is the product of an enzymatically processed precursor. CORT precursors are encoded by two different genes that evolved from a common ancestral gene by a duplication mechanism. processing of CORT precursor generates diverse mature peptides as CORT-14 and -29 in rodents and CORT-17 and -29 in humans.
Although CORT was initially discovered in the brain and it is especially abundant in the cortex (where its name comes from), further reports showed that this neuropeptide is also widely distributed at peripheral tissues including gastrointestinal tract and pancreas. Based on its ability to activate ssts, CORT exhibits almost endocrine and most non-endocrine actions of SST. Actually, their main functional divergences, reside in the ability of CORT to promote sleep functions, modulate locomotor activity, exert potent anti-inflammatory actions in experimental models of inflammatory and autoimmune disorders and, its influence on atherogenesis[1].
Cortistatin (CORT) shares high structural and functional similarities with somatostatin (SST)They share some biological activities, some distinct biological activities that are not shared between them, for example some central actions. This evidence suggested the existence of a specific CORT receptor; indeed, differently from SST, CORT is able to bind to Mas-related gene X (MrgX)-2 receptor in various central and peripheral as well as in some neoplastic tissues. Moreover, CORT but not SST is also able to bind the GH secretagogs receptor (GHS-R) that mediates endocrine and non-endocrine actions of ghrelin, its natural ligand. However, the physiological relevance, if any, of CORT binding to these receptors is still unknown[2].
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[1]Chanclón B, Martínez-Fuentes AJ, Gracia-Navarro F. Role of SST, CORT and ghrelin and its receptors at the endocrine pancreas. Front Endocrinol (Lausanne). 2012, 3:114
[2]Giordano R, Picu A, Bonelli L. The activation of somatostatinergic receptors by either somatostatin-14 or cortistatin-17 often inhibits ACTH hypersecretion in patients with Cushing’s disease. Eur J Endocrinol. 2007,157(4):393-398.
