Somatostatin, also known as growth hormone-inhibiting hormone (GHIH).
Somatostatin is secreted by delta cells at several locations in the digestive system, namely the pyloric antrum, the duodenum and the pancreatic islets.
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 exerts its inhibitory effects.
Somatostatin release from delta cells can act in a paracrine manner.
In the stomach, somatostatin acts directly on the acid-producing parietal cells via a G-protein coupled receptor.
Somatostatin inhibits adenylate cyclase, thus effectively antagonizing the stimulatory effect of histamine to reduce acid secretion.
Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones, including gastrin and histamine which effectively slows down the digestive process.
A peptide hormone that regulates the endocrine system and affects neurotransmission and cell proliferation via interaction with G protein-coupled somatostatin receptors and inhibition of the release of numerous secondary hormones.
Somatostatin works to stop the pituitary gland from releasing certain hormones, including growth hormones and thyroid-stimulating hormones.
Somatostatin is produced by neuroendocrine neurons of the ventromedial nucleus of the hypothalamus.
These neurons project to the median eminence, where somatostatin is released from neurosecretory nerve endings into the hypothalamohypophysial system through neuron axons.
Somatostatin is then carried to the anterior pituitary gland, where it inhibits the secretion of growth hormone from somatotrope cells.
The somatostatin neurons in the periventricular nucleus mediate negative feedback effects of growth hormone on its own release.
Somatostatin neurons respond to high circulating concentrations of growth hormone and somatomedins by increasing the release of somatostatin, so reducing the rate of secretion of growth hormone.
It inhibits insulin and glucagon secretion.
Chromosome 3.
Somatostatin has two active forms produced by the alternative cleavage of a single preproprotein: one consisting of 14 amino acids,the other consisting of 28 amino acids.
Humans have only one somatostatin gene, SST.
Somatostatin is secreted by delta cells at several locations in the digestive system, namely the pyloric antrum, the duodenum and the pancreatic islets.
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.
Somatostatin release from delta cells can act in a paracrine manner.
It acts in the stomach, directly on the acid-producing parietal cells via a G-protein coupled receptor antagonising the stimulatory effect of histamine to reduce acid secretion.
Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones, including gastrin and histamine, effectively slowing down the digestive process.
Biliary disease is a common side effect of somatostatin analogues, with a frequency ranging from 10-63%.
As somatostatin analogues are the mainstay of neuroendocrine tumor treatment, it is associated with a high incidence of biliary stone disease.
Somatostatin is produced by neuroendocrine neurons of the ventromedial nucleus of the hypothalamus.
These neurons of the ventromedial nucleus project to the median eminence, where somatostatin is released from neurosecretory nerve endings into the hypothalamohypophysial system.
Somatostatin receptors are expressed at many different sites in the brain:
arcuate nucleus, the hippocampus, and the brainstem nucleus of the solitary tract.
Somatostatin is then carried to the anterior pituitary gland, where it inhibits growth hormone secretion from somatotrope cells.
The somatostatin neurons in the periventricular nucleus mediate negative feedback effects of growth hormone.
Somatostatin neurons respond to high circulating concentrations of growth hormone y increasing the release of somatostatin, so reducing the rate of secretion of growth hormone.
Somatostatin is also produced by several other areas of the brain, and somatostatin receptors are expressed at many different sites in the brainwashing well.
Populations of somatostatin neurons occur in the arcuate nucleus, the hippocampus, and the brainstem nucleus of the solitary tract.
Somatostatin is classified as an inhibitory hormone.
Somatostatin is induced by low pH.
Its release is inhibited by the Vagus nerve.
In the anterior pituitary gland, the effects of somatostatin are:
Inhibiting the release of growth hormone (GH)
Opposes the effects of growth hormone–releasing hormone (GHRH))
Inhibiting the release of thyroid-stimulating hormone (TSH)
Inhibiting adenylyl cyclase in parietal cells.
Inhibiting the release of prolactin (PRL).
Somatostatin suppresses the release of gastrointestinal hormones :
Decreases the rate of gastric emptying,
Reduces smooth muscle contractions and blood flow within the intestine,
Suppresses the release of pancreatic hormones.
Somatostatin release is triggered by the beta cell peptide urocortin3, thereby
inhibiti g insulin release.
Somatostatin I nhibits the release of glucagon, and suppresses the exocrine secretory action of the pancreas.
((Octreotide)) is an octapeptide that mimics natural somatostatin pharmacologically.
Octreotide is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone.
Octreotide has a much longer half-life than somatostatin, about 90 minutes, compared to 2–3 minutes.
It is administered parenterally -subcutaneously, intramuscularly, or intravenously, as it is poorly absorbed orally.
It is indicated for symptomatic treatment of carcinoid syndrome, acromegaly, and polycystic diseases of the liver and kidney.
((Lanreotide)) medication is used in the management of acromegaly and symptoms caused by neuroendocrine tumors, most notably carcinoid syndrome.
Lanreotide is a long-acting analog of somatostatin, like octreotide.
Somatostatin analogues are associated with exocrine pancreatic insufficiency in the majority of patients.
Octreotide is absorbed poorly from the gut, and is therefore administered parenterally: subcutaneously, intramuscularly, or intravenously.
It is indicated for symptomatic treatment of carcinoid syndrome and acromegaly.
It is used in polycystic diseases of the liver and kidney.
Lanreotide is used in the management of acromegaly and symptoms caused by neuroendocrine tumors, most notably carcinoid syndrome.
It is a long-acting analog of somatostatin, like octreotide.
Common adverse events for somatostatin analogues include: nausea, abdominal pain, diarrhea, steatorrhea, flatulence, hyperglycemia, and biliary sludging.