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Somatostatin is secreted by delta cells at several locations in the digestive system, namely the pyloric antrum, the duodenum and the pancreatic islets. [14]Somatostatin released in the pyloric antrum travels via the portal venous system to the heart, then enters the systemic circulation to reach the locations where it will exert its inhibitory effects.
In both species, the peptide hormone Urocortin III (Ucn3) is a major local signal that is released from beta cells (and alpha cells in primates) to induce the local secretion of somatostatin. [3] It has also been suggested that somatostatin may be implicated in insulin-induced hypoglycaemia through a mechanism involving SGLT-2 receptors.
Effects of somatostatin. Somatostatin is a G protein-coupled receptor ligand. When the receptors are activated, it causes the cells where the receptors are expressed to decrease hormone secretion. [2]
Affects gut motility; increases jejunal and ileal fluid secretion Pancreatic polypeptide: Pancreas: Inhibits pancreatic and biliary secretion Peptide YY: Colon: Inhibits food intake Somatostatin: Stomach, pancreas: Inhibits secretion and action of many hormones Substance P: Enteric nerves: Unclear Trefoil peptides: Stomach, intestine: Mucosal ...
Hormones secreted include somatostatin, motilin, cholecystokinin, neurotensin, vasoactive intestinal peptide, and enteroglucagon. [10] The enteroendocrine cells sense the metabolites from intestinal commensal microbiota and, in turn, coordinate antibacterial, mechanical, and metabolic branches of the host intestinal innate immune response to ...
Somatostatin receptor antagonists (or somatostatin inhibitors) are a class of chemical compounds that work by imitating the structure of the neuropeptide somatostatin, which is an endogenous hormone found in the human body. The somatostatin receptors are G protein-coupled receptors.
Also inhibits the secretion of pancreatic polypeptide. [18] A large number of G protein-coupled receptors (GPCRs) regulate the secretion of insulin, glucagon, and somatostatin from pancreatic islets, [19] and some of these GPCRs are the targets of drugs used to treat type-2 diabetes (ref GLP-1 receptor agonists, DPPIV inhibitors).
Histamine and gastrin act synergistically as the most important stimulators of hydrochloric acid secretion from parietal cells and stimulators of secretion of pepsinogen from chief cells. The most important inhibitor of the ECL cell is somatostatin from oxyntic D cells.