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Query: UNIPROT:P01350 (gastrin)
9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum gastrin increased in patients with pernicious anaemia after a beef-meal, but decreased after an oral load of glucose, xylose or sodium chloride. 50 g of glucose and 25 or 75 g of xylose suppressed serum gastrin to approximately 40% of basal values at 60 min and were slightly more effective than 10 g of sodium chloride. There was no rise in beef-meal stimulated serum gastrin concentration in vagotomized patients and only a slight rise in two patients with duodenal ulcer when an oral dose of 10 g of sodium chloride was given together with the beef-meal. 25 g of xylose suppressed basal serum gastrin concentration significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in all subjects examined. Further studies indicated, however, that vasopressin was only effective when pharmacological plasma concenten orally and intraduodenally were compared in six patients with pernicious anaemia. Serum gastrin concentration decreased approximately to the same extent in both experiments. It is concluded that the inhibitory effect of glucose on gastrin secretion most likely is mediated hormonally via osmo-receptors located in the small intestine.
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PMID:Inhibition of gastrin secretion by hypertonic solutions in patients with pernicious anaemia and duodenal ulcer. 11 45

The concentration and molecular form of gastrin in urine were determined radioimmunochemically. Urine from hypergastrinaemic patients (Zollinger-Ellison syndrome and pernicious anaemia) contained gastrins corresponding to the serum components I and II. The excretion of gastrin increased with increasing gastrin concentrations in serum. Urine from six subjects with normal concentrations of gastrin in serum contained "apparent" gastrin immunoreactivity which could not be removed by specific immunoabsorption. No gastrin was detectable by gel filtration of desalted and concentrated urine from normal subjects. The apparent immunoreactivity was due partly to interference by sodium chloride. The results indicate that hypergastrinaemic patients, in contrast to normal subjects, excrete gastrins in the urine.
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PMID:Immunochemical studies on gastrins in the urine. 36 Dec 96

Liquid test meals were infused into the stomach and acid secretion was measured by intragastric titration at pH 5.0 Acid secretion after 500 or 750-ml sodium chloride meals was two to three times higher than basal secretion rates and was equivalent to 25-30% of the peak acid output in response to histamine. Since these meals did not cause a rise in serum gastrin concentration, it is assumed that they stimulate acid secretion by causing distention of the body and fundus of the stomach. Compared with this distention stimulus, glucose meals had no effect on acid secretion and fat-inhibited acid secretion; however, both glucose and fat caused an increase in serum gastrin concentration. Amino acids caused a much greater increase in serum gastrin concentration and enhanced acid secretion above that noted with distention alone. In contrast, albumin did not enhance the serum gastrin concentration or stimulate acid secretion to a statistically significant extent. There was a close correlation between the rise in serum gastrin concentration and rate of acid secretion after different test meals when average results for each test meal were plotted. However, there was a poor correlation between acid secretion and serum gastrin concentration when the responses of the individual subjects with a given test meal were compared. Our interpretations are: (a) Distention is an important stimulant of the acid-secretory response to a meal, and this is not mediated by gastrin release. (b) Gastrin is one but probably not the only mediator of the chemical phase of acid secretion, i.e., acid secretion noted with amino acids that cannot be explained by distention. (c) Glucose and fat also release gastrin; however, with glucose the rise in serum gastrin is too small and too transient to enhance acid secretion, and fat probably releases unmeasured inhibitors that overwhelm the effect of gastrin on acid secretion. (d) Albumin is not a stimulant of acid secretion.
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PMID:Studies on the mechanisms of food-stimulated gastric acid secretion in normal human subjects. 95 91

Two strains of rat, Sprague-Dawley and inbred Piebald Virol Glaxo pigmented (PVG) strain, were dosed orally with hypertonic sodium chloride at a dose of 0.25, 0.5, 1.0 or 1.33 g/kg. Gastric epithelial cell proliferation was compared 16 hours after a single dose. The rats were given intraperitoneal bromodeoxyuridine (20 mg/kg) 1 hour before sacrifice, and cells undergoing DNA synthesis (S-phase) were assessed using a monoclonal antibody to bromodeoxyuridine. The number of labelled cells per gastric gland was counted using video image analysis, assessing ten low-power fields (160-180 gastric glands) per rat. Tissue injury was graded for submucosal oedema, inflammation and necrosis; it was minimal after dosing with 0.25 and 0.5 g/kg of sodium chloride. The PVG rats were more susceptible to tissue injury after dosing with 1.0 or 1.33 g/kg of sodium chloride: submucosal oedema, 80% in the PVG and 10% in the Sprague-Dawley; inflammation, 70% compared with 10%; necrosis, 70% compared with 20%. The number of labelled cells per fundic gland increased with increasing dose concentration of sodium chloride and the response was similar for both strains of rat. Plasma gastrin concentration at the time of sacrifice was significantly higher in the PVG rat for the 0.5, 1.0 and 1.33 g/kg doses. These strain differences may be useful in the further evaluation of the mechanisms of sodium chloride-induced tissue damage and repair.
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PMID:Gastric epithelial cell proliferation and histological damage after hypertonic sodium chloride: the effect of variation in the strain of rat. 157 Dec 83

In this study the effect of Nac1 on plasma immunoreactive gastrin was investigated. I.P. administration of sodium chloride (0.9%) in a dose of 1 ml/kg.b.w. for 7 days in rats, produced a significant rise in level of sodium ion in plasma. This hypernatraemia was also accompanied by significant rise in values of plasma immunoreactive gastrin. The mechanism(s) of this sodium chloride-induced release of gastrin is discussed.
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PMID:Sodium chloride-induced hypergastrinaemia in rats. 180 Jun 26

The study was designed to obtain information on selected extrapulmonary effects of enprofylline, an adenosine-non-blocking alkylxanthine that is about 5 times more potent as a bronchodilator than the adenosine receptor antagonist theophylline. Effects of theophylline (5.0 mg/kg) on lower esophageal sphincter pressure (LESP), gastric secretion, and diuresis and of enprofylline (1.5 mg/kg intravenously producing about 2 micrograms/ml plasma) were examined in 8 healthy volunteers. Enprofylline and theophylline decreased LESP (by 5.0 +/- 2.6 mm Hg, mean +/- SD, p less than 0.001, and by 5.8 +/- 2.7 mmHg, p less than 0.001, respectively), but only theophylline stimulated gastric secretion (volume p less than 0.01 and acidity p less than 0.01) and urine production (volume p less than 0.01 and sodium chloride excretion p less than 0.01). Neither xanthine affected plasma gastrin. Enprofylline and theophylline can be expected to have a similar ability to reduce the barrier to gastroesophageal reflux, but only the latter would have additional stimulant effects on gastric secretion and diuresis. These findings may have clinical significance and suggest a role for adenosine in regulating gastric secretion (and diuresis) but not LESP.
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PMID:Relaxation of lower esophageal sphincter and stimulation of gastric secretion and diuresis by antiasthmatic xanthines. Role of adenosine antagonism. 396 10

The effect of salmon calcitonin (SMC) on pancreatic enzymes and hormones was investigated following retrograde choledocho-pancreatography (ERCP). 40 patients were randomly divided in two groups and 2.5 micrograms/h SMC or sodium chloride was infused intravenously for 28 hours. Infusion was started 4 hours before endoscopic procedure and amylase, lipase, glucose, insulin, glucagon and gastrin plasma concentrations were measured before and 2, 12 and 24 hours after the end of the ERCP. According to the radiological findings of pancreatography two additional groups were formed: group 1 with visualization of the main duct and its branches and group 2 with additional visualization of the pancreatic parenchyma. No change in glucose, insulin, glucagon and gastrin was found in any of the groups analyzed. Amylase and lipase showed a significant increase after 2 hours and 24 hours later, values were reached which were not significantly different to baseline levels. The time course of the plasma concentrations was identical in the patients treated by SMC or sodium chloride and showed no significant difference at the various time intervals. Therefore, inhibition of the known increase in pancreatic enzymes following ERCP was not found with SMC treatment.
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PMID:[The effect of salmon calcitonin on pancreatic enzymes and hormones before and after retrograde cholangiopancreatography]. 616 82

A comparison was made between use of isotonic 0.15 M sodium chloride and 5.8 g/100 ml glucose solutions for measurement of gastric acid secretion by intragastric titration in normal and ulcer subjects. Glucose distention did not cause significantly different acid secretion than saline distention in either group. The total amounts of glucose entering the duodenum over the 3.5-hr study period were 99 g in normal subjects and 122 g in ulcer subjects. In normal subjects, circulating gastrin-related acid secretion curves were not significantly different during endogenous peptone and exogenous G-17 stimulation using either the glucose or the saline meals. This finding provides evidence that glucose meals of this size do not alter sensitivity to gastrin. With glucose meals, inhibition of gastric emptying caused retention of a sufficient volume in the stomach to permit accurate continuous intragastric titration. Saline meals caused pronounced diarrhea which was not seen after glucose meals. Glucose distention intragastric titration allows reliable comparisons of endogenously and exogenously stimulated gastric acid secretion without serious side effects and is especially suitable for studying acid secretion in duodenal ulcer subjects.
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PMID:Glucose perfusion intragastric titration. 670 44

Fasting gastrointestinal motor and hormone patterns were studied in 11 healthy volunteers. Cyclic motor activity was present in all subjects during fasting, but the duration and site of onset of each cycle were variable, even in the same subject. Fasting gastrin, GIP, and glucagon levels remained low and constant during the 8-hr study, while plasma motilin levels exhibited cyclic variation in 7 of the 11 subjects. Achlorhydria (induced with cimetidine in 5 of the 11 subjects) did not alter the pattern of fasting motor activity or plasma motilin. In the remaining six subjects, the effect of liquid nutrient meals was examined. Ingestion of a sodium chloride bolus failed to disrupt fasting cyclic activity, while all nutrient-containing solutions inhibited gastric phase-2 motor activity, the duration of inhibition being longest for the mixed and lipid meals. All nutrient meals released GIP, while only protein and mixed meals released gastrin, and the lipid meal released motilin. Our study confirms the rhythmicity of interdigestive motor cycles in man and demonstrates their lack of dependence on gastric acid secretion and some relationship to motilin cycles in certain individuals as determined by radioimmunoassay. Transition from fasting to fed pattern (after liquid meals) is characterized by the inhibition of phasic gastric pressure changes in the antrum and the development of irregular activity in the intestine, similar in pattern to fasting phase 2. Because the duration of interruption of the gastric interdigestive pattern by meals depends on their nutrient content, we conclude that dietary composition may be a major determinant of the fasting-fed motor balance in man.
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PMID:Human interdigestive and postprandial gastrointestinal motor and gastrointestinal hormone patterns. 706 84

Gastric stress ulcers were produced by restraint in nonsecretory rats, and the response of the ulcer index to intraduodenal hydrochloric acid (HCl) or sodium chloride (NaCl) was studied in a three-step dose-response trial. Both substances lowered the ulcer index dose-dependently (Km HCl 0.038 +/- Km NaCl 0.089 +/- 0.009 mM/kg/h, respectively) reaching a nadir in rats receiving HCl. The improvement in ulcerations was associated with elevated plasma secretin, glucose, and lowered gastrin in this protocol. In both experimental procedures plasma vasoactive intestinal peptide (VIP) was higher with the low and intermediate doses as compared with the high dose when a slight venous hyperosmolality was present. Glucagon and insulin remained essentially stable. It is concluded that stress ulcers of the restraint type may be prevented by intraduodenal HCl, suggesting that the interplay of gastrointestinal hormones is deranged by stress and partly restored by acid instillation.
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PMID:Gastric stress ulcers and gastrointestinal hormones - response to hydrochloric acid and sodium chloride infused intraduodenally. Preliminary report. 721 4


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