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)

Intracerebroventricular (icv) injection of pentagastrin showed a powerful, dose dependent antidipsogenic effect in the rat. Drinking behavior stimulated by 48 h water deprivation was inhibited by 2000 ng of pentagastrin which also blocked, at lower doses, water intake induced by icv injection of angiotensin II (100 ng) and carbachol (150 ng). Pentagastrin was less effective on food intake stimulated by 24 h starvation. The antidipsogenic effect was not a consequence of behavioral alteration. It is suggested that gastrin-like peptides in the brain may play a role in the regulation drinking, acting as thirst inhibitors.
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PMID:Effect of intracerebroventricular injection of pentagastrin on rat drinking behavior. 408 Jun 44

1. Enzyme secretion in response to short duration vagal stimulation or to rapid I.V. injections of cholecystokinin-pancreozymin (CCK-PZ) or gastrin or to intra-arterial injections of acetylcholine is a function of the volume of juice secreted and not primarily a function of time.2. The output of amylase in response to each stimulus occurred in a constant volume of approximately 15 drops (0.5 ml.) regardless of the rate of background secretin stimulated flow of water and electrolyte.3. It is argued that because amylase secretion occurs in this constant volume, it is due to the rapid secretion of enzyme into the duct system from the acini, and subsequently the secretin stimulated secretion of water and bicarbonate washes the enzyme from the duct system.4. When enzyme secretion is stimulated an increase in the electrical conductance (measured at 1.592 kHz) occurs across the tail of the pancreas. This increased conductance has two components. An early peak associated with the extrusion of enzyme from the acinar cell and a later peak which is probably due to vasodilatation.5. Atropine was without effect on both enzyme secretion and the conductance record when the stimulant was CCK-PZ. Atropine blocked enzyme secretion and both peaks of the conductance record in response to stimulation by acetylcholine. Atropine blocked enzyme secretion and abolished the early phase of the conductance record, on vagal stimulation. It was without effect on the later peak which probably indicates an atropine resistant vasodilation of the pancreatic vessels.6. When the vagus is stimulated on a background of submaximal electrolyte secretion caused by the intravenous infusion of secretin, the volume rate of secretion and the rate of amylase secretion follow a similar time course. The maximal volume response occurred between 7 Hz and 15 Hz and the maximal amylase output per impulse was at 5 Hz.
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PMID:The kinetics of pancreatic amylase secretion and its relationship to volume flow and electrical conductance in the anaesthetized cat. 485 25

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.
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PMID:Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine. 513 20

Cholecystokinin (CCK)-like immunoreactivity (CCK-LI) in a pool of 12 dog brains was extracted sequentially into boiling water and cold 2% trifluoroacetic acid. Gel filtration on Sephadex G-50 revealed three main molecular forms detected by a carboxyl-terminal antibody; one was eluted in the position of CCK-58 (58 amino acid residues long); a second, in the position of CCK-8; and a third, near the radioactive iodide marker. When the CCK-LI was purified by affinity chromatography using carboxyl-terminal CCK antibody followed by three steps of reversed-phase high-pressure liquid chromatography, three components were isolated and characterized by sequence microanalysis. The smallest component was the pentapeptide common to gastrin and CCK. The second peak was eluted in the same region as synthetic CCK octapeptide, and sequence analysis showed that the chemical structure of this biologically active region of canine CCK is identical to that found in sheep and pig brains. The 22-residue amino-terminal sequence of brain CCK-58 was: Ala-Val-Gln-Lys-Val-Asp-Gly-Glu-Pro-Arg-Ala-His-Leu-Gly -Ala-Leu-leu-Ala-Arg-Tyr-Ile-Gln-, the same as the sequence found for canine intestinal CCK-58 from this pool of dogs. This is the same sequence others have reported for porcine brain CCK-58 lacking nine amino acid residues (CCK-58 desnonapeptide) except that the porcine peptide had a serine in position 9. The canine CCK amino-terminal sequence differed from the sequence Ala-Gln-Lys-Val-Asn-Ser previously reported for intestinal CCK-58 purified from another pool of dog tissue, but the rest of the residues identified were identical in the two peptides. CCK-58 may be a molecular precursor of the smaller forms of CCK in brain as well as in gut.
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PMID:Isolation of a large cholecystokinin precursor from canine brain. 609 6

Cholecystokinin, bombesin or gastrin (2 microliter of 50 ng/microliter) was injected stereotaxically into the paraventricular nucleus of the hypothalamus, the arcuate/ventromedial area, the subfornical organ, the area postrema and the cerebral aqueduct of Sprague-Dawley rats and the effects of these injections on food and water intake were studied. While the injection of cholecystokinin reduced food intake when it was injected into both hypothalamic loci, food and water intake were most severely affected by the injection of this peptide into the cerebral aqueduct. Bombesin reduced food intake after its injection into all areas except the subfornical organ and reliable reductions in water intake were seen after injection of this peptide into all areas except the paraventricular nucleus. Minor reductions in food intake were seen following gastrin injection into the paraventricular nucleus while increased water consumption was observed after this peptide was injected into the paraventricular nucleus and cerebral aqueduct. In a second study 6-hydroxydopamine injections (2 microliter of 8 micrograms/microliter were made into the five areas studied 10 days before animals were injected with 100 micrograms/kg of cholecystokinin (i.p.). All 6-hydroxydopamine-injected animals reduced their food and water intake in response to the cholecystokinin challenge as did intact controls. These results indicate that while the changes in food and water intake produced by the central injection of cholecystokinin, bombesin or gastrin may involve central catecholamine systems, those occurring after its systemic administration do not. Therefore, if the release of gastrointestinal peptides during natural feeding is part of a homeostatic mechanism regulating hunger and satiety, this mechanism may operate without directly involving central catecholamine systems.
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PMID:Ventricular, paraventricular and circumventricular structures involved in peptide-induced satiety. 609 74

The mechanisms by which somatostatin inhibits acid secretion when infused into the lumen of the stomach have been examined in 20 healthy subjects. The acid secretory response to distension with 500 ml of neutral water was examined in nine successive 10-min test periods in each subject. Samples of serum and boiled neutral gastric juice were collected and frozen for later immunoassay for gastrin. Somatostatin was added to the distending fluid in a concentration of 600 pg/ml in the middle 3 test periods in 10 test subjects, and placebo added in the same 3 test periods in 10 control subjects. The addition of somatostatin inhibited the rate of acid secretion as compared with placebo alone in the control subjects (p < 0.025) without altering the concentration of immunoreactive gastrin in the serum but reducing the concentration of immunoreactive gastrin in gastric juice (p < 0.02). The data are consistent with the suggestions that the intraluminal administration of somatostatin inhibits antral gastrin release in a paracrinic manner and inhibits acid secretion indirectly by inhibiting lumina gastrin-mediated acid secretory activity.
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PMID:Effect of luminal somatostatin on acid secretion and gastrin release. 610 87

Fifteen male Holstein X Frisian calves, weighing 65 +/- 3 kg and fed a milk replacer twice daily were fitted with a return cannula loop, chronically implanted at 10 days of age in the pancreatic duct, were used. In six successive experiments we have observed the influence of an intravenous infusion of secretin, cholecystokinin pancreozymin (CCK-PZ), vasoactive intestinal peptide (VIP), glucagon, gastrin and somatostatin on pancreatic juice flow rate, and on the excretion of proteins, calcium, inorganic phosphorus, zinc and amylase activity of pancreatic juice. In two other experiments, we have studied the interaction of secretin (or CCK-PZ) with somatostatin (SRIF). Each experiment was performed 5 h after calves feeding and no milk was given to the animals during the time of sampling. Our results indicate that the endocrine regulation of the exocrine pancreas in young calves is similar to that described in other mammals. Secretin and CCK-PZ increased significantly excretion of water, calcium, magnesium, inorganic phosphorus, zinc, proteins and amylase activity. Somatostatin and glucagon inhibited effects observed with two precedent hormones. Gastrin increased pancreatic juice flow rate but excretion of protein and amylase activity do not varied significantly. VIP showed no significant effect on pancreatic excretion of water, minerals, proteins and amylase activity. However, our animals seem to be characterized by a more intense excretion of proteins and amylase in the pancreatic juice following secretin than after CCK-PZ infusion.
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PMID:The endocrine regulation of exocrine pancreas in preruminant milk-fed calves. 610 15

The effects of somatostatin, instilled into the duodenum or administered intravenously, on pancreatic response to endogenous (meal and duodenal acidification) or exogenous (secretin and caerulein) stimulants were compared in five dogs with gastric and pancreatic fistulas. Somatostatin, whether applied topically to the duodenal mucosa or given intravenously, resulted in qualitatively similar inhibition of pancreatic secretion of water, bicarbonate, and enzyme protein, being about four to eight times less potent after intraduodenal than after intravenous administration. A meal-induced secretion appears to be the most sensitive to the inhibitory action of intraduodenal somatostatin, probably because of the suppression of gastric acid and serum gastrin secretin involved in the postprandial stimulation of the exocrine pancreas. The inhibition of pancreatic secretion by luminal somatostatin was accompanied by a significant increase of plasma levels of the immunoreactive somatostatin, indicating that this peptide can be absorbed intact across the intestinal mucosa. We conclude that somatostatin administered into the gut lumen is absorbed into the circulation and can inhibit pancreatic secretion both by the suppression of the release of gastrointestinal hormones and by direct inhibitory action on the exocrine pancreas.
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PMID:Studies on the inhibition of pancreatic secretion by luminal somatostatin. 611 84

1. In order to assess if proximal enterectomy induces changes in the function of the exocrine pancreas, the exocrine pancreas was studied 1 week, 4 weeks, and 6 months after 50 or 75% proximal small bowel resection. 2. One week after 50 and 75% proximal small bowel resections, basal pancreatic bicarbonate outputs, studied by means of an external pancreatic fistula in conscious rats, were increased significantly over control values by 43 and 78% respectively. Four weeks after a 75% resection, the bicarbonate output was still significantly higher in resected animals than in sham operated animals. 3. The increase of volume and bicarbonate of the basal pancreatic secretion coincided with a 4-fold increase in plasma secretin concentration 1 week after resection. Both increased pancreatic secretion and plasma secretin concentration were transient. 4. The pancreatic hypersecretion was specifically reversed to control values with an I.P. injection of jejunoileal mucosa homogenate. 5. Serum gastrin and somatostatin values in intestinal mucosa and pancreas were not changed 1 and 4 weeks after enterectomy compared with sham operated animals. 6. The weight of the pancreas and its content of DNA were unaltered by resection. Amylase and chymotrypsinogen per gram pancreatic tissue and per microgram DNA were reduced 4 weeks following resections as compared with sham operated rats. After 6 months, chymotrypsinogen appeared further reduced in resected animals. 7. It is concluded that extensive proximal enterectomy in rats produced early, transient and marked increases in basal pancreatic water and bicarbonate secretion and in plasma secretin due to the loss of jejunoileal inhibitor(s), and a selective decrease in certain enzymes in pancreatic tissue.
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PMID:Exocrine pancreatic function following proximal small bowel resection in rats. 612 11

In dogs gastric secretion induced by tetragastrin and pancreatic secretion induced by secretin and/or cholecystokinin were inhibited by somatostatin at doses of 0.06-1 microgram X kg-1 X h-1 and 0.06-1 microgram X kg-1 X 0.5 h-1, respectively. Inhibition was a linear function of the logarithm of dose. Basal and 2-deoxy-D-glucose-induced gastric acid secretion was also significantly inhibited by low doses of somatostatin. Results in this study differ from those reported previously by clarifying the action of somatostatin as follows. 1) The inhibitory effect of somatostatin on pancreatic protein secretion was significantly greater than that on water and bicarbonate production. Somatostatin was more effective on cholecystokinin- than secretin-induced pancreatic secretion. 2) Although gastric mucosal blood flow (MBF) was affected by somatostatin, the reduction of MBF was not the primary mechanism responsible for its inhibitory action. 3) The low doses of somatostatin used in this study significantly inhibited gastric and pancreatic secretion without affecting the basal plasma concentrations of insulin, glucagon, growth hormone, gastrin, or secretin in the dogs, suggesting that the inhibitory action was not mediated by changes or reduction in plasma concentration of these hormones.
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PMID:Action of somatostatin on stomach, pancreas, gastric mucosal blood flow, and hormones. 612 5


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