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

Endoscopic manometry of sphincter of Oddi (SO) and serum levels of gastrin, glucagon, and somatostatin were measured in patients with postcholecystectomy syndrome (n = 12), asymptomatic cholecystectomy patients (n = 6), and controlled subjects (n = 14). Pentagastrin-stimulated gastric acid secretion test was also performed in part of patients who had symptoms or no symptoms after the removal of gallbladder. The results showed that the patients of symptomatic group had hypertonic dyskinesia of SO as shown by deep and wide waves superimposed on high basal pressure plateau of SO. The symptomatic group also had a higher serum level of gastrin and a greater BAO than those of other two groups. No difference of serum levels of glucagon and somatostatin was found among these three groups. The hypertonic dyskinesia of SO and hypergastrinemia are possibly important factors in the pathogenesis of postcholecystectomy syndrome.
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PMID:[A study on motility of sphincter of Oddi in postcholecystectomy syndrome]. 191 67

Intravenous infusion of pentagastrin increases salivary secretion progressively at doses from 1 to 4 micrograms/kg body weight/h. Pentagastrin also stimulates salivary secretion of amylase. Simultaneous administration of somatostatin, at the dose that inhibits gastric secretion of pentagastrin-stimulated HCl, blocks the effect of pentagastrin on salivary flow, while it does not reduce the amylase concentration. The data suggest that different mechanisms underlie the effects exerted by pentagastrin on salivary flow and on the concentration of amylase in saliva.
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PMID:Effect of somatostatin on salivary secretion in man. 243 64

This study investigates release of somatostatin-like immunoreactivity (SLI) into the gastric lumen of five healthy human subjects in response to pharmacological stimuli (pentagastrin and secretin) and physiological stimuli (sham feeding and intrajejunal perfusion of elemental diet). Basal and poststimulation gastric juice aspirates were collected at 15-min intervals, extracted with acetone, and SLI determined by radioimmunoassay, with these results: A considerable amount of SLI was secreted during the basal period. Pentagastrin stimulated SLI release quickly and was associated with increased acid secretion. Both secretin and sham feeding increased SLI only slightly. During intrajejunal perfusion of the elemental diet, SLI increased significantly, was associated with decreased acid secretion, and rapidly returned to basal level when elemental diet was replaced by saline. Basal levels of gastric luminal SLI thus showed distinct changes in response to each stimulus. Although the physiological action of luminal SLI remains to be studied, its levels may reflect gastric D-cell activities.
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PMID:Luminal gastric somatostatin-like immunoreactivity in response to various stimuli in man. 287 75

To further investigate differences in the responses of normals and patients with duodenal ulcer with respect to gastrin release and acid and pepsin secretion, we infused bombesin (1 microgram/kg X h) or bethanechol (40 micrograms/kg X h) during the middle hour of a 3-h infusion of pentagastrin and compared the results with a pentagastrin infusion without added drug. Pentagastrin dosage (0.1 microgram/kg X h) was set to give about half-maximal response, to detect either inhibition or further stimulation of gastric secretion, whereas the dose of bombesin was chosen to give maximal gastrin but less than maximal acid secretion. Serum gastrin and somatostatin were also measured. In all subjects tested, bethanechol produced no effects on acid, gastrin, or somatostatin release but increased pepsin output. By contrast, bombesin inhibited pentagastrin-stimulated acid output in all 6 normal men by an average of 55%, whereas it inhibited acid output in only 2 of the 9 men with duodenal ulcer. Serum gastrin increases after bombesin in duodenal ulcer were three to four times greater than in normals. Although bombesin stimulates acid only by releasing gastrin, we postulate that bombesin may also simultaneously limit acid and pepsin secretion and speculate that this effect could be mediated by bombesin-induced somatostatin release. The cause for differences between duodenal ulcer and normal remain speculative.
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PMID:Divergent effects of bombesin and bethanechol on stimulated gastric secretion in duodenal ulcer and in normal men. 288 66

The aim of our study was to examine the direct effect of somatostatin on histamine- and pentagastrin-stimulated intrinsic factor (IF) release in collagenase-dispersed guinea pig gastric glands. The effect of somatostatin (10(-11) M to 10(-6) M) on half-maximal doses of histamine (10(-6) M), pentagastrin (10(-6) M), and both histamine and pentagastrin together was tested. All tested concentrations of histamine significantly stimulated IF release. Pentagastrin (10(-10) M to 10(-6) M) inconsistently stimulated IF release. The quantity of IF release stimulated by histamine and pentagastrin together was approximately the additive sum of that produced by either agent alone. Somatostatin (10(-6) M) inhibited histamine-stimulated (10(-6) M) IF release by 69.9 +/- 7.2% and the combination of histamine (10(-6) M) and pentagastrin (10(-6) M) by 64.2 +/- 9.1%. This is the first in vitro demonstration that somatostatin inhibits IF release.
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PMID:Somatostatin inhibition of intrinsic factor secretion from isolated guinea pig gastric glands. 288 25

A humoral mechanism, potentiating the maximal acid, but not the pepsin response to exogenous gastrin in cats, is activated by protein-rich food in the stomach or duodenum, but not in the jejunum. In the present study, the effect of an oral meat meal on the maximal acid response to pentagastrin was investigated in Heidenhain pouch (HP) cats, and in antrectomized HP cats with duodenal exclusion and gastrojejunostomy Rouxen-Y. Antrectomy and duodenal exclusion abolished the postprandial HP acid response, and feeding did not potentiate the acid response to pentagastrin. The finding suggests that the gastrin-potentiating mechanism in the stomach is localized in the antrum, and it cannot be demonstrated in the jejunum. The basal plasma levels of gastrin and somatostatin did not differ in antrectomized and non-antrectomized cats. Antrectomy and duodenal exclusion abolished the postprandial gastrin and somatostatin responses. The plasma somatostatin increase during pentagastrin infusion persisted after antrectomy and duodenal exclusion. It is concluded that the antrum is not mandatory for the basal plasma levels of gastrin and somatostatin, but the postprandial gastrin response is of antral origin and may release somatostatin. Pentagastrin infusion releases extra-antral somatostatin in cats.
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PMID:Antrum participates in the postprandial augmentation of the acid response to exogenous gastrin in conscious cats. 288 10

The purpose of this study was to determine whether the inhibitory action of peptide YY (PYY) on gastric acid secretion is attributable to the release of gastric somatostatin in rats. Two groups of rats (six rats/group) were anesthetized with urethane and prepared with gastric fistulas and jugular catheters. Pentagastrin (18 micrograms/kg-h) was given intravenously for 150 min to stimulate gastric acid secretion. Intravenous PYY (130 micrograms/kg-h) inhibited pentagastrin-stimulated gastric acid secretion significantly (P less than 0.05). Administration of iv PYY resulted in a 41% reduction (P less than 0.05) in pentagastrin-stimulated gastric acid secretion. In another group of anesthetized rats, administration of PYY (10(-7), 10(-8) M) failed to stimulate a release of somatostatin from the isolated-perfused rat stomach. Our findings indicate that PYY can inhibit gastric acid secretion independently of release of gastric somatostatin in the rat.
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PMID:Inhibition of gastric acid secretion by peptide YY is independent of gastric somatostatin release in the rat. 290 61

We studied in five healthy volunteers whether the cholinergic pathway regulated the secretion of gastric intraluminal somatostatin-like immunoreactivity (SLI) in response to stimuli of pentagastrin infusion (0.9 micrograms/kg/h, intravenously) and sham feeding. We measured gastric secretory volume, hydrogen ion output, and SLI at base line, during pentagastrin infusion, after sham feeding, and after applications of atropine (0.0, 0.7, 7.0 micrograms/kg, intramuscularly) given before pentagastrin and sham feeding. The stimuli were given randomly, at separate times on different days. After each stimulus, eight 15-min gastric juice collections were made; samples were adjusted to pH 7, pepstatin-A and aprotinin were added, and samples were extracted with acetone to determine SLI by radioimmunoassay. Pentagastrin and sham feeding significantly increased gastric luminal SLI secretion, which appeared to correlate with the increases in volume and acid output. Atropine at 7 micrograms/kg significantly suppressed gastric volume, acid, and SLI outputs stimulated by sham feeding; however, responses to pentagastrin stimulation remained unchanged. To conclude, the cholinergic mechanism regulates gastric intraluminal SLI response to sham feeding but not to pentagastrin infusion.
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PMID:Mechanism of release of gastric luminal somatostatin-like immunoreactivity in response to pentagastrin and sham feeding in man. 343 15

The effects of 1 and 4 micrograms/kg/h somatostatin on pentagastrin-stimulated gastric mucosal blood flow and acid secretion were investigated in 12 normal subjects and in 12 patients with cirrhosis of the liver. Each dose of somatostatin was given intravenously to six normal subjects and to six patients. Gastric mucosal blood flow was measured by the neutral red clearance of the stomach. Pentagastrin at a dose of 0.67 micrograms/kg/h stimulated acid secretion less in patients with cirrhosis of the liver than in normal subjects. In normal subjects 1 micrograms/kg/h somatostatin induced a parallel decline of gastric mucosal blood flow and gastric secretion; with 4 micrograms/kg/h somatostatin mucosal blood flow was inhibited more than gastric secretion. In patients with cirrhosis of the liver gastric mucosal blood flow remained unaffected by both doses of somatostatin, while acid secretion was slightly decreased. It is concluded that somatostatin can affect gastric mucosal blood flow independently of acid secretion. Somatostatin may be ineffective in the treatment of gastric haemorrhage in patients with cirrhosis of the liver.
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PMID:Somatostatin reduces gastric mucosal blood flow in normal subjects but not in patients with cirrhosis of the liver. 613 13

Infusion of gastrin, G-17I, at 0.4 microgram/min into either the maternal or fetal venous circulation of six late gestation sheep was associated with increases in serum gastrin concentration in the infused circulation and reciprocal decreases in the serum gastrin concentration in the other circulation (contraplacental) that perfused the placenta. Pentagastrin infusion at 0.4 microgram/min was associated with an increase in C-terminal specific gastrin immunoreactivity in both the infused and the contraplacental circulations. These observations suggest that biologically active fragments of gastrin, but not the intact molecule, may cross the ovine placenta. An alternative explanation for our results is that gastrin infusion into either the maternal or fetal circulation which perfuses the placenta may result in the release of an inhibitor (i.e., somatostatin) into the other circulation. Of broad importance, these observations indicate that although intact polypeptide hormones may not traverse the placenta, their concentrations in maternal and fetal sera may not be as independent as previously believed. Serum gastrin half-life values in late gestation sheep fetuses, lambs, and ewes were determined to be 13.7 +/- 1.9, 16.7 +/- 2.6, and 15.2 +/- 2.8 min, respectively. These similar values indicate that the relatively high serum gastrin concentrations observed in near-term sheep fetuses are not the result of prolonged half-life in the fetus.
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PMID:Contraplacental hypogastrinemic effect of gastrin infusion in sheep. 673 92


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