Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The different mode of secretion of the gut hormones (paracrine secretion--somatostatin. endocrine and neurocrine secretion--gastrin, CCK; neurocrine secretion--VIP, substance P), obscures the physiological significance of these hormones. However, the pathophysiological role of autonomous secreted hormones by endocrine tumours, is well established. Gut hormones are used for routine evaluation of gastrointestinal diseases. The therapeutic value of these substances has recently engendered considerable interest.
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PMID:[Pathophysiology and clinical significance of gut hormones]. 4 99

The effect of somatostatin on secretin-, CCK-pancreozymin-and-carbachol-stimulated pancreatic secretion was studied in eight healthy volunteers. In all instances there was a significant reduction in duodenal secretory volume after secretin without any change in bicarbonate concentration. CCK-parcreozymin and carbachol stimulated volume and enzyme secretion were significantly inhibited and gallbladder contraction was abolished by somatostatin. In three volunteers a reversible hypercoagulation during infusion of 200 mug/h cyclic somatostatin has been observed. Somatostatin inhibited the CCK-pancreozymin stimulated pancreatic enzyme secretion of anaesthesized rats.
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PMID:Inhibition by somatostatin of pancreatic juice and enzyme secretion and gallbladder contraction induced by secretin, cholecystokinin-pancreozymin and carbachol administration. 6 52

The chemistry, localisation, release and effects of gastrointestinal hormones and some related peptides are surveyed. Their main presumed physiologic actions are: gastric acid and pepsin secretion are stimulated by gastrin and to a less degree by secretin. Acid secretion is inhibited by bulbo-enterogastrone and GIP. Biliary water and electrolytes are augmented by gastrin, CCK-PZ, secretin and VIP and inhibited by Substance P. Pancreatic bicarbonate and enzyme secretions are stimulated by secretin and CCK-PZ, especially in combination. Lower oesophageal and antral motility and tonus are elevated following gastrin and motilin; the gallbladder and small intestine empty following CCK. Gastrin regulates gastrointestinal, and CCK pancreatic, tissue growth. Somatostatin inhibits all gut hormones. All peptides are vasoactive within the splanchnic area, each one in a specific manner.
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PMID:Gastrointestinal hormones. 35 98

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.
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PMID:Effect of somatostatin on bile-induced acute hemorrhagic pancreatitis in the dog. 39 59

With a view toward the therapeutic use of somatostatin in the treatment of acute pancreatitis, a preliminary investigation was conducted with 6 healthy volunteers, in which the suppressive effect of somatostatin on endocrine and exocrine pancreatic function was observed. A 30-minute baseline measurement period was followed by the administration of cyclic somatostatin (100 microgram by i.v. injection plus a 90-minute infusion at a rate of 200 microgram/hr). After the first 45 minutes of this infusion secretion was submaximally stimulated by the infusion of secretin-cholecystokinin-pancreozymin (CCK-PZ) (75 U each), over two hours. No decrease was observed in basal bicarbonate or enzyme concentration under somatostatin administration alone. However, secretion did not show the usual steep rise after the commencement of stimulation. After the somatostatin infusion was stopped, i.e. under secretin-CCK-PZ alone, a significant increase occurred in the values of secretin-induced volume, bicarbonate concentration and total bicarbonate contents of the duodenal aspirate, as well as in CCK-PZ-induced enzyme secretion. The release of insulin, both basal and stimulated, was also significantly decreased by somatostatin.
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PMID:[Suppressive effect of somatostatin on secretin-CCK-PZ-stimulated endocrine and exocrine pancreatic function in man (author's transl)]. 41 Jan 66

The effect of linear somatostatin on pancreatic exocrine secretion in anaesthetized rats has been studied. Basal secretion of amylase was significantly inhibited by an infusion of 100 microgram/100 g/h somatostatin, but increased fourfold after a bolus injection of 50 microgram/100 g. CCK-stimulated enzyme and volume secretion were inhibited by somatostatin. Somatostatin did not influence secretin-stimulated bicarbonate concentration or rate of secretion in the dose range in which enzyme secretion was inhibited.
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PMID:Effect of somatostatin on basal and stimulated pancreatic secretion in the rat. 64 Feb 71

A further specific, reproducible radioimmunoassay of cholecystokinin-pancreozymin was developed. 125J-labelled 39-CCK was used as tracer. The limit of detection for CCK in serum was 40 pg/ml. Basal levels for CCK have been found to be 222 pg/ml, being increased after food ingestin. No crossreactivity with gastronintestinal hormones could be observed. Somatostatin was inhibiting the stimulated CCK-release. Histochemical and radioimmunological determinations localized CCK-containing cells in duodenal tissue of humans. Physiological and pathological processes in which CCK is involved have to be studied to evaluate its role in the gastrointestinal tract.
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PMID:[Radioimmunoassay [RIA] of cholecystokinin-pancreozymin [33-CCK] (author's transl)]. 65 86

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.
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PMID:[New views on gastrointestinal hormones]. 85 99

Gastrointestinal hormones are considered to be those that are formed in the gastrointestinal tract and there, in physiological concentrations, develop their effects on motility, secretion, trophism, bloodflow and absorption. Structural analysis, synthesis or a high degree of purity after extraction, and its exact demonstration by means of a useful radioimmunoassay, form the basis for the establishment of a polypeptide as a gastrointestinal hormone. To this category belong, at the present time, gastrin, cholecystokinin-pancreozymin (CCK-PZ) and secretin. GIP, VIP, motilin, glucagon and somatostatin are considered likely candidates. The substances gastrin and CCK-PZ, which are structurally related and have a predominantly stimulating effect, and the structurally dissimilar motilin, contrast with the partially or totally inhibiting hormones of the glucagon family, namely, secretin, VIP, glucagon-enteroglucagon, GIP and somatostatin. By the combined action of these hormones with one another and with the autonomic nervous system, the digestive processes are regulated. Disturbances in the formation of these hormones, in particular an overproduction, give rise to disease syndromes that can now be diagnosed and, in part, treated by surgery. The therapeutic application of gastrointestinal hormones has now also become a possibility.
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PMID:[Gastrointestinal hormones]. 96 Sep 54

The effect of the neuropeptide galanin on insulin and somatostatin secretion in the rat was studied under various conditions. In the perfused rat pancreas, insulin secretion stimulated by arginine, but not cholecystokinin-8 (CCK-8) or acetylcholine (ACh) was inhibited by both rat and porcine galanin, whereas ACh-stimulated somatostatin release was inhibited by rat but not porcine galanin. Neither arginine nor CCK-8 significantly altered somatostatin secretion and galanin was without effect under those conditions. Gastric inhibitory polypeptide-stimulated insulin release from cultured mixtures of purified rat beta- and non-beta-cells was inhibited by rat and porcine galanin in a concentration-dependent and equipotent manner. The results suggest that the inhibitory effect of galanin on insulin and somatostatin secretion may be stimulus-specific and species-specific.
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PMID:Stimulus-specific inhibition of insulin release from rat pancreas by both rat and porcine galanin. 128 Jul 55


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