Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of gastrin and secretin were measured in experimental animals and in man following gastric surgery. Serum gastrin was higher in the fasting, and increased further after test meal in proximally gastrectomized subjects as compared in those receiving total gastrectomy and in normal controls. Serum secretin level, however, was unchanged before and after test meal irrespective to two surgical procedures. Dogs undergoing proximal gastrectomy showed increased output of bicarbonate and amylase as an exocrine pancreatic secretion after instillation of 0.1N HCl into the duodenum. Increased DNA synthesis was observed in the small intestine and pancreas in the proximally gastrectomized dogs. Therefore, higher level of serum gastrin may possess trophic activity in animals undergoing proximal gastrectomy. The findings obtained in this study suggest that we should select, if possible, the proximal gastrectomy leaving the antral region from the view point of trophic action of gastrointestinal hormones.
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PMID:[Serum gastrin and secretin and their trophic action after proximal and total gastrectomy]. 408 34

After prolonged fasting the activity of histidine decarboxylase in the oxyntic mucosa of the rat stomach is low. Feeding or injection of gastrin or insulin rapidly raises the enzyme activity. It was earlier suggested that all enzyme-activating agents act through release of gastrin. This view has found experimental support in studies which show that in antrectomized rats the enzyme is activated by gastrin but not by gastrin-releasing stimuli like feeding or vagal excitation (insulin hypoglycemia). In the present investigation rats were subjected to a variety of treatments and serum gastrin concentrations and gastric histidine decarboxylase activities were measured. The main findings were as follows.1. Feeding raised the serum gastrin level and the enzyme activity in unoperated rats. In fasted antrectomized rats the serum gastrin concentration was low; in freely fed antrectomized rats it was at the same level as in fasted unoperated rats. In antrectomized rats the enzyme activity was low and not raised by feeding.2. Acid in the antrum inhibits the release of gastrin whereas an alkaline pH may facilitate such release. All treatments that blocked acid secretion, thereby raising the antral pH, also raised the serum gastrin concentration and concomitantly the histidine decarboxylase activity. Thus, vagotomy increased the serum gastrin level and the histidine decarboxylase activity in fasted rats. Treatment of fasted unoperated rats with atropine or hexamethonium had similar effects. Antral exclusion, which prevents HCl from reaching the pyloric glands, resulted in marked increase in the serum gastrin concentration and in the enzyme activity of fasted rats.3. Injection of insulin resulted in a rather slow, progressive increase in the serum gastrin concentration. The peak was reached after about 4 hr. The enzyme activity was also raised markedly and the peak response occurred about 1 hr later.4. An increase in the histidine decarboxylase activity was invariably preceded or accompanied by a raised serum gastrin level. With fasted or fed unoperated, vagotomized, antrectomized or antrally excluded rats, the correlation coefficient for the relation between enzyme activity and serum gastrin concentration was 0.69 (P < 0.05).5. Porta-caval-shunted fasted rats responded to feeding or injection of insulin with marked activation of gastric histidine decarboxylase. The response after feeding was at least 5 times higher in shunted than in nonshunted rats but serum gastrin was only slightly higher. Following antrectomy of porta-caval-shunted rats feeding no longer raised the enzyme activity. Thus, the enzyme-activating agent was of antral origin. In the shunted rats injection of pentagastrin induced an enzyme activation about 5 times that seen in intact rats. This response was not significantly reduced by antrectomy. In conclusion, we have observed a correlation between serum gastrin concentration and histidine decarboxylase activity. We have failed to obtain evidence for the existence of any physiological intermediate other than gastrin in the activation of histidine decarboxylase induced by feeding, vagal stimulation or inhibition of acid secretion.
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PMID:Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity. 444 71

Intraluminal manometric studies were carried out in 19 patients with untreated achalasia and in 20 normals. Lower esophageal sphincter (LES) pressure was 50.5 +/-4.6 mm Hg in patients with achalasia as compared with 19.4 +/-1.3 mm Hg in the normal group. In both groups, the LES pressure was lowered when exogenous 0.1 N HCl was placed into the stomach. Although the nadir of pressure attained with acid suppression was the same, the per cent inhibition was significantly greater in patients with achalasia. Serum gastrin levels were the same in the two groups studied. The patients with achalasia, pre- and postpneumatic dilatation, showed a supersensitivity to exogenous intravenous gastrin I, as compared with normals. These data suggest that high, acid-suppressible levels of LES pressure, in patients with achalasia, are due to supersensitivity to endogenous gastrin.
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PMID:Role of gastrin supersensitivity in the pathogenesis of lower esophageal sphincter hypertension in achalasia. 557 32

Experiments were performed on conscious dogs with chronic pouches of the antrum, the duodenal bulb or the ileum, which were perfused with solutions of varying pH. Gastrin and somatostatin levels were measured in the perfusates. When the pouches were perfused with 0.15 M NaCl only small amounts of gastrin and somatostatin (1 pmol/min) were released into the lumen of the antrum and of the duodenal bulb. By lowering pH of the perfusion fluid a pH dependent release of somatostatin was induced into the lumen of the antrum and the duodenal bulb. Perfusion with 0.1 M HCl caused a large output of somatostatin (6--60 pmol/min) into the pouches. The upper pH limit for stimulation of the intraantral or intrabulbar somatostatin release appeared to be approximately pH 3--4. Somatostatin was also released into ileal perfusates at intraluminal pHs below 3--4. Lowering of pH in the antral pouches caused an increased intraluminal gastrin release, which was quantitatively less impressive than that of somatostatin. Occasionally also the gastrin release into the duodenal bulb increased during perfusion with 0.1 M HCl, whereas no such release was induced by acidification of the lumen of the ileum. It is suggested that the inhibition of gastrin release observed at low intraantral pH is mediated by a local effect of somatostatin, since this peptide is released in a pH dependent manner in the antropyloric region. It is also suggested that acidification of any region of the gastrointestinal tract will stimulate the release of peptides from all endocrine cells of the open type, probably by an unspecific effect on the membrane. Thus both gastrin and somatostatin are released by acidification of the antrum, but in the presence of high local levels of somatostatin, the release of gastrin is substantially inhibited.
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PMID:Effect of intraluminal pH on the release of somatostatin and gastrin into antral, bulbar and ileal pouches of conscious dogs. 611 41

Somatostatin and gastrin release into the gastric lumen was investigated in anaesthetized, vagally intact rats. The stomach was perfused at a flow rate of 0.5 mL.min-1. During perfusion with 0.1 M HCl or buffers of varying pH the somatostatin ans gastrin concentrations in the perfusate were less than 10 pg.mL -1 and approximately 30 pg.mL-1, respectively. Peptone caused a gastrin concentrations in the perfusate were less than 10 pg.mL-1 and approximately 30 pg.mL-1, respectively. Peptone caused a slight pH-independent increase in somatostatin release; gastrin release was unchanged despite an increase in serum gastrin from a basal of 15 +/- 4 to 155 +/- 34 pg.mL-1 during peptone stimulation. intravenous infusion of carbachol (1 microgram.kg-1.min-1) strongly stimulated luminal somatostatin and gastrin release (from 5 +/- 1 to 192 +/- 52 pg.mL-1 and from 27 +/- 5 to 198 +/- 41 pg.mL-1, respectively) during perfusion with 0.1 M HCl. Phosphate buffer perfusion at pH 7.5 abolished the cholinergic-mediated somatostatin release but the gastrin response was unaffected. It is suggested that changes of luminal hormone concentrations in the rat stomach do not reflect the secretory activity of the endocrine cells in the gastric mucosa.
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PMID:Somatostatin and gastrin release into the gastric lumen in rats. 611 61

1. Gastric emptying and secretion were measured in conscious calves during alkaline or acid perfusion of the duodenum with simultaneous assessment of endogenous plasma somatostatin, gastrin and blood 5-hydroxytryptamine (5-HT).2. Alkaline duodenal perfusion (isotonic NaHCO(3)) caused rapid gastric emptying and increased gastric acid secretion without any affect on basal levels of somatostatin, 5-HT or gastrin.3. Duodenal perfusion of 60 mm-HCl caused complete inhibition of gastric emptying, reduced gastric acid secretion considerably, and an associated elevation of somatostatin basal levels from 123.8 +/- 11.2 to 281.9 +/- 23.0 pg/ml. (P < 0.01) occurred.4. These effects of duodenal perfusion were unimpaired by bilateral lumbar splanchnectomy.5. On bilateral cervical vagotomy of the splanchnectomized calves, the inhibition of gastric function evoked by duodenal acidification persisted, and plasma somatostatin showed a further significant elevation to 506.9 +/- 49.9 pg/ml. (P < 0.01) but gastrin and 5-HT remained unchanged. The increased gastric function caused by alkaline duodenal function was significantly reduced following vagotomy but basal somatostatin, gastrin and 5-HT in the blood remained unaffected.6. These results suggest that the stimulatory effect on gastric emptying and acid secretion of isotonic NaHCO(3) in the duodenum may be mediated, partially at least, through the vagal nerves but not the splanchnics.7. The complete inhibition of gastric function which ensued on acidification of the duodenum and which continues after splanchnovagotomy, is not mediated by the autonomic nervous system. This inhibitory process appears to involve the endocrine system only, with somatostatin (but not gastrin or 5-HT) fulfilling a main enterogastrone role.
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PMID:Intestinal control of gastric function in the calf: the relationship of neural and endocrine factors. 612 10

The influence of the autonomic nervous system on the secretion of somatostatin from the antral and the fundic parts of the stomach and from the pancreas of the pig was investigated in experiments involving electrical stimulation of the vagal nerves and the splanchnic nerves in (1) intact, anesthetized pigs and (2) isolated perfused preparations of (a) antrum with intact vagal supply, (b) pancreas with intact vagal supply, (c) pancrease with intact sympathetic supply. The results clearly demonstrated that parasympathetic activity inhibits D-cell function in all gastro-pancreatic tissues; antral gastrin secretion was inversely correlated to somatostatin secretion and it is suggest that antral D-cell secretion participates in the control of gastrin secretion; the inhibitory effect of Gastric Inhibitory Polypeptide (GIP) as well as intraluminal HCl on gastrin secretion may be exerted via the stimulatory effect of both on somatostatin secretion. The sympathetic innervation of the pancreas is also clearly inhibitory to the pancreatic somatostatin secretion, whereas sympathetic nervous activity influences little the gastric somatostatin release.
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PMID:Nervous control of gastro-pancreatic somatostatin secretion in pigs. 612 87

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49 +/- 10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49 +/- 10 to 23 +/- 9 pM, whereas gastrin and insulin levels rose from 9 +/- 2 and 140 +/- 14 pM to 48 +/- 11 and 370 +/- 91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin level rose again and peaked at around 60 min after feeding (110 +/- 24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCl secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.
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PMID:Plasma levels of somatostatin following a test meal in dogs. Initial atropine resistant vagally mediated decrease of somatostatin levels and increase of gastrin and insulin levels. 612 67

The porcine antrum was isolated with the pancreas and perfused in vitro with an artificial medium supplemented with erythrocytes. The vagal innervation was preserved. Effluent was collected from the portal vein as well as from a vein directly draining the antrum. Electrical vagal stimulation increased gastrin output and inhibited somatostatin output. Intraluminal hydrochloric acid had the opposite effect. Gastric inhibitory polypeptide (GIP) in physiological concentrations (90 and 450 pmol/l) increased somatostatin output, inhibited gastrin output, and potentiated the effect of HCl on somatostatin release. Vagal stimulation, however, abolished the GIP effect on somatostatin output. Thus gastrin and somatostatin outputs were always inversely affected by the applied stimuli, suggestive of somatostatin-mediated control of gastrin secretion. GIP may exert its effects via local somatostatin release.
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PMID:Effect of vagus, gastric inhibitory polypeptide, and HCl on gastrin and somatostatin release from perfused pig antrum. 613 53

Newborn dogs, humans, and rats have elevated gastric luminal pH values and significantly elevated serum gastrin levels compared to adults. In the adult, acidification of the antral mucosa to pH 3.0 or lower inhibits gastrin release. Somatostatin is released by acid and may mediate this effect. We examined the effects of gastric acidification and somatostatin injection in rats aged 10 days to adult. Gastric gavage with 0.15 M HCl significantly lowered serum gastrin in animals of all ages. Somatostatin injection (400 micrograms/kg) significantly decreased serum gastrin in rats aged 18 days or older, but not in 10- and 15-day-old animals. These data indicate that 1) the mechanism whereby antral acidification inhibits gastrin release is at least partially developed in unweaned rats, 2) somatostatin is not a necessary mediator of the inhibition of gastrin release, and 3) at least part of the hypergastrinemia found in newborn animals is of antral origin.
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PMID:Effects of somatostatin and acid on inhibition of gastrin release in newborn rats. 614 32


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