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)

Measurements of serum cortisol and gastrin along with gastric acid-pepsin secretion in the resting state were carried out in gastric and duodenal ulcer patients. Increased basal corticosteroid concentrations were observed in patients with duodenal ulcer and gastric ulcer. Higher concentrations of the hormone were observed in the former group (P less than 0.05 for the latter). Fasting gastrin levels were significantly higher in gastric ulcer patients where gastric secretion is low than those in duodenal ulcer patients (P less than 0.001). These results suggest that the effect of adrenal cortical hormone on lowering the threshold of oxyntic gland cell reactivity against gastrin is an important factor in duodenal ulcer etiology. Extra-antral control mechanism(s) of gastric acid-pepsin secretion should not be overlooked.
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PMID:Characteristics of adrenocortical function, gastrin release and gastric secretion in duodenal ulcer etiology. 38 39

The stomachs of six healthy volunteers were intubated with a Levine tube. In addition, a thin polyethylene tube was placed in the proximal jejunum or in the proximal duodenum. After a 1-h period with no perfusion the intestine was perfused for 2 h with 7% liver extract (LE) (pH 5.5; 380 MOsm/kg water) at a rate of 100 ml/h. In control tests 200 ml of 0.9% physiologic saline solution were used as perfusate. Reflux to the stomach was determined by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin levels were measured in 15-min periods. During perfusion of the proximal jejunum only pepsin outputs were increased significantly. During duodenal perfusion of LE, gastric acid and pepsin outputs were increased to 31% and 73% of maximal pentagastrin stimulation, respectively. Controls showed no changes in gastric secretion. Plasma gastrin levels were not elevated after jejunal or duodenal perfusion. These results confirm that the intestinal phase of gastric secretory stimulation does exist in humans. Furthermore, it appears that the major portion of this stimulation originates from the duodenum and is not gastrin-dependent.
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PMID:Comparison of gastric secretory response in man to duodenal and jejunal liver extract perfusion. 38

In 10 healthy subjects and 25 duodenal ulcer patients, gastric acid and pepsin and serum gastrin responses to cephalic-vagal stimulation induced by modified sham-feeding (MSF) were studied before and after vagotomy and atropinisation and compared with those to maximal stimulation with pentagastrin. When the MSF-induced peak acid output was normalised as a percentage of peak response to pentagastrin it was about 62% in healthy subjects and 66% in duodenal ulcer patients. Serum gastrin concentration was not changed significantly by modified sham-feeding either in normal subjects or in duodenal ulcer patients. Truncal vagotomy completely abolished gastric acid and pepsin responses to MSF in duodenal ulcer patients. Atropine almost completely suppressed gastric acid and pepsin responses to MSF in healthy subjects and reduced those in duodenal ulcer patients by about 62%. The combination of the modified sham-feeding and pentagastrin infusion resulted in augmentation of the acid output in duodenal ulcer patients but not in healthy subjects. This study shows that the cephalic phase results in a potent gastric acid and pepsin stimulation which is not accompanied by any change in serum gastrin concentration either in healthy subjects or duodenal ulcer patients and which is abolished by vagotomy and suppressed by atropine.
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PMID:Cephalic phase of gastric secretion in healthy subjects and duodenal ulcer patients: role of vagal innervation. 39 56

Three dogs were surgically prepared with gastric fistulas and Heidenhain (vagally denervated) pouches. Acid and pepsin responses to pentagastrin and food were determined before, at the end of a 1-mo period of total parenteral feeding, and 1 mo after the resumption of a normal oral diet. Acid and pepsin output from the denervated pouch in response to pentagastrin and food decreased significantly (P less than 0.001) after parenteral feeding and returned to control levels after the dogs resumed a normal diet. Secretory outputs from the gastric fistula in response to pentagastrin remained unchanged throughout the experiment. Basal serum gastrin levels decreased 50% during the period of intravenous feeding and returned to levels approximately twice the control levels following resumption of normal oral food intake. Serum gastrin responses to a meal also decreased during intravenous alimentation and returned to higher than normal levels following a 1-mo period of oral intake. These studies indicate that the absence of oral food intake in the dog does not result in decreased acid secretion from the innervated stomach. Vagal innervation in some way is responsible for the preservation of normal secretion during the absence of food from the gastrointestinal tract of the dog.
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PMID:Effect of long-term parenteral feeding on gastric secretion in dogs. 40 83

To study the relation between gastrin released by vagal excitation and the secretion of H+ and pepsin under various conditions, central vagal excitation was induced by 2-deoxyglucose (2DG) in doses of 50, 100, and 200 mg/kg body wt given as a single intravenous injection in seven gastric fistula dogs, three with fundic vagotomy and four with intact vagi. Serum gastrin increased linearly with dose doubling in both groups but was twice as high in the vagotomized dogs. Total acid output for 3 h was related linearly to integrated gastrin output in both groups, but the slope, H+/gastrin, was 10 times steeper in the vagally intact dogs (330 vs. 34 mueq/pg gastrin-ml-30 min) and pepsin output almost 20 times greater [5,400 peptic units (PU) vs. 296 PU]. Acidification of the antrum to pH 1.2-1.4 eliminated the gastrin response to 2DG in both groups of dogs. Atropine (100 microgram/kg iv) reduced serum gastrin in the vagotomized and increased it in the intact dogs. Atropinization uncovers stimulation by 2DG by pathways that do not involve muscarinic cholinergic receptors. Stimulation by both pathways is suppressible by acid. We conclude that fundic vagotomy removes an inhibitor of vagal gastrin release.
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PMID:Augmented vagal release of antral gastrin by 2-deoxyglucose after fundic vagotomy in dogs. 42 Feb 87

This study tested the hypothesis that the inhibitory action of secretin on gastrin-stimulated gastric acid and pepsin secretion is comprised in animals harboring intestinal stages of the parasite Trichinella spiralis. Pentagastrin-stimulated acid and pepsin secretion, and the influence of secretin on these processes, were measured in dogs prepared with gastric fistulas and Heidenhain pouches. Dogs were studied before and after infection with 10(4) T. spiralis larvae/kg body weight. Gastric secretion was stimulated by constant intravenous infusion of pentagastrin, 1 microgram/kg per hour. Exogenous secretin inhibited pentagastrin-stimulated acid and pepsin output from both the main stomach and Heidenhain pouch in infected as well as in the uninfected dogs. Identical inhibition was observed in uninfected dogs during duodenal infusion with HCl to release endogenous secretin. In contrast, duodenal stimulation with HCl did not inhibit acid and pepsin secretion in dogs tested during the 1st week following infection. Results support the conclusion that the regulatory effect of secretin on gastrin-stimulated gastric secretion is impaired during the early phase of infection, and is due to depressed synthesis or release of secretin from duodenal mucosa.
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PMID:Influence of parasitism on secretin-inhibited gastric secretion. 48 66

In rats the influence of arresting free motions (= controls; mild stress) and of restraint (= severe stress) without and with additional somatostatin (SRIF) on gastric secretion, mucosal microcirculation and stress ulcer formation was studied. Severe stress alone reduces volume, acid and pepsin secretion, acid concentration, aminopyrine clearance and ratio. The ulcer index is elevated. Under both conditions SRIF inhibits in a dose-dependent manner volume and acid secretion, and ulcer incidence is lower. The interaction between severe stress and the antiulcer component of SRIF is characterized as non-competitive. Under these conditions and a continuous infusion of SRIF (10.0 microgram/kg.h over 8 h) acid concentration, acid and pepsin secretion fall subtotally, ulcer index to 50 percent of vehicle (saline) treated rats, if gastric fistula drains juice outside stomach. Microcirculation and serum gastrin are unchanged. In animals with closed fistula ulcer index is reduced by 85 percent, average gastrin again is unchanged. It is concluded that stress ulcers develop at a low secretory and microcirculatory state of gastric mucosa. The prophylactic effect of SRIF results from direct inhibition of parietal and chief cells and additional yet unknown factors.
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PMID:Anti-stress ulcer and anti-secretory effect of somatostatin in rats -- failure to suppress serum gastrin. 56 56

In 23 volunteers with gastric hyperchlorhydria the effect of intravenous administration of salmon calcitonin (SMC) on basal (n = 11) and pentagastrin-stimulated gastric secretion (n = 12) and on immunoreactive serum gastrin (n = 11) was studied under various experimental conditions. SMC (0.075 microgram . kg(-1) . 2h(-1) and 0.3 microgram . kg(-1) . h(-1)) caused a statistically significant reduction of HCl output of 75% and 80% and of pepsin of 55% and 90%. Serum gastrin concentration showed a dose-dependent decrease of 17% and 31% respectively. Pentagastrin-stimulated acid secretion was moderately inhibited by short-term administration of SMC (0.15 and 0.30 microgram . kg(-1) . 30 min(-1)), the effect being confined to the period of application of the hormone. Long-term infusion of the smaller dose for 2 1/2 h induced a sustained decrease of HCl output by 55%. It is assumed that SMC inhibits gastric secretion mainly by interfering with the production or liberation, or both, of gastrin. Whether long-term administration of SMC has advantages over substances currently used as therapeutic inhibitors of gastric secretion, e.g. in gastroduodenal bleeding, has yet to be investigated.
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PMID:Response of basal and pentagastrin-stimulated gastric secretion and of serum gastrin to short- and long-term intravenous infusion of salmon calcitonin in hyperchlorhydric subjects. 56 55

The inhibitory effects of cimetidine on gastric acid and pepsin secretion were studied before and after 1 month of treatment with 300 mg of cimetidine four times a day in 15 male duodenal ulcer patients. Cimetidine inhibited both pentagastrin- and peptone meal-stimulated acid secretion significantly better before, than after, 1 month of treatment. Similarly cimetidine inhibited pentagastrin-stimulated pepsin secretion significantly better before treatment. Meal-stimulated serum gastrin concentrations were significantly higher after treatment. The mechanism(s) of these effects was not apparent.
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PMID:Effect of one-month treatment with cimetidine on gastric secretion and serum gastrin and pepsinogen levels. 62 Sep 8

VIP and secretin were compared in regard to their effects on gastric acid and pepsin secretion induced by pentagastrin histamine or a peptone meal as well as on gastric mucosal blood flow and meal induced serum gastrin level in conscious dogs provided with gastric fistulas and denervated fundic pouches. Both VIP and secretin caused a dose-related stimulation of basal pepsin outputs and inhibition of pentagastrin-induced acid secretion. VIP, like secretin, inhibited pentagastrin and meal-induced gastric acid secretion but in contrast to secretin it caused inhibition of acid response to histamine. Inhibition of acid secretion by VIP or secretin was accompanied by secondary reduction in gastric mucosal blood flow in tests with pentagastrin or histamine and by depression of the serum gastrin level in tests with a peptone meal. This study indicates that in comparison with secretin, VIP has a wider spectrum of inhibition of stimulated gastric secretion and may be considered as one of the enterogastrones released in the small intestine.
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PMID:Comparison of vasoactive intestinal peptide (VIP) and secretin in gastric secretion and mucosal blood flow. 76 58


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