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)

Gastrin antisera were raised by immunization of rabbits or guinea pigs with synthetic human gastrin I conjugated to bovine serum albumin by carbodiimide. Radioiodination of SHG: 2-17 was performed by the chloramine T-method and by an enzymatic procedure. AE-cellulose was used to get a monoiodinated tracer hormone. Antibody reactions with the different forms of gastrin and with CCK-PZ was characterized. Precision (VK = 6-8%) and reproducibility (VK less than 15%) of the gastrin values were comparable to the insulin assay. Gastrin stimulates the parietal cell and has trophic effects on gastric mucosa. Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum-syndrome which are due to autonomous gastrin release. Some findings suggest a pathogenetic role of gastrin in duodenal ulcer disease. Those disease in which gastrin determinations are of clinical value are discussed.
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PMID:[Gastrin]. 65 84

The effect of dopamine infusion on basal and pentagastrin-stimulated gastric secretion, on basal and secretin-CCK-PZ-stimulated pancreatic secretion, and on basal and meal-induced gastrin release has been evaluated in healthy volunteers. Both basal and stimulated gastric acid secretion were significantly inhibited during dopamine infusion with a significant rebound to pre-infusion values after discontinuing dopamine. These effects were prevented by pretreatment with the antidopaminergic drug, metoclopramide. A slight but now significant decrease in amylase and bicarbonate outputs was also observed during dopamine infusion, while gastrin release did not change. These data suggest the existence of dopaminergic mechanisms in the regulation of gastric acid secretion in man.
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PMID:Effect of dopamine infusion on gastric and pancreatic secretion and on gastrin release in man. 68 Jun 4

Pressure responses to cholecystokinin (CCK-PZ, approximately 500 U/mg) and gastrin (human synthetic gastrin) were investigated in isolated guinea-pig antral and fundal pouches. Both drugs stimulated motor activity, in the antrum mainly by increasing amplitudes and rhythmic activity, in the fundus by increasing basal tension. Antral responses to gastrin were markedly smaller than to CCK-PZ, while the differences were less pronounced in the fundus. Prestimulation with gastrin, being an agonist by itself, significantly reduced the antral responses to submaximal doses of CCK-PZ, while no inhibition was found in the fundus. When pre-exposed to gastrin, the antral dose-response curve to CCK-PZ was flattened, with reduced maximal response, simulating a non-competitive interaction. It seems that gastrin behaves like a partial agonist to CCK-PZ on guinea-pig antral smooth muscle.
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PMID:Interactions of cholecystokinin (CCK-PZ) and gastrin on motor activity of isolated guinea-pig antrum and fundus. 72

Synthesis of gastrin, CCK-PZ-octapeptide sulphate ester and secretin, is dealt with in some detail. A gastrin synthesis developed by the author's team is also described. The synthesis of glucagon and caerulein is, though touched upon, but not discussed in any detail.
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PMID:Synthesis of gastrointestinal peptide hormones. 80 96

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.
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PMID:[New views on gastrointestinal hormones]. 85 99

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.
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PMID:[Gastrointestinal hormones. I. Hormones of the gastrin group]. 87 Oct 64

In five dogs with chronic gastric fistulas (Thomas cannula) and a new type of chronic pancreatic fistula which permits collection of pure nonactivated pancreatic juice after ingestion of a test meal, the following series of experiments were performed: In the first series, a test meal (400 gm. canned dog meat) was given with 200 ml. saline simultaneously infused through the gastric cannula. In response to this stimulus, the 20-minute peak pancreatic flow rate and bicarbonate output were respectively 33% and 34%, of the maximal secretion of the pancreatic gland obtained with secretin in six control dogs provided with gastric and the classical Thomas duodenal fistula. The 20-minute peak protein output represented 84% of the maximal secretory capacity attained with dose-response curves to CCK in the same group of control animals. In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged. It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity, and unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described.
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PMID:Canine exocrine pancreatic secretory changes induced by an intragastric ethanol test meal. 87 Nov 15

1 Intracellular recordings of membrane potentials and input resistance have been made from the exocrine acinar cells of mouse and rat pancreas placed in a tissue bath perfused with Krebs-Henseleit solution.2 The resting acinar cell membrane potential was about -38 mV. The acinar cells were stimulated by cholecystokinin-pancreozymin (CCK-PZ), gastrin and the gastrin-related polypeptides, caerulein and desulphated caerulein. The immediate effect of stimulation with these secretagogues was always a depolarization and a concomitant reduction in input resistance and time constant. Depolarization of the acinar cell membrane by these secretagogues was not abolished in the presence of atropine (1.4 muM).3 These peptide secretagogues were divided into the gastrin group and the CCK-PZ group according to the time course of the depolarizations and the shape of the dose-response curve. The depolarization evoked by the gastrin group returned quickly to the resting level but that evoked by the CCK-PZ group was long lasting. The time course and the dose-response curve for desulphated caerulein was identical with that of gastrin.4 It was confirmed electrophysiologically that the activity of gastrin is exerted by the C-terminal tetrapeptide; but the activity of caerulein depends on the C-terminal heptapeptide, especially the presence in the molecule of the sulphated tyrosyl residue at position 7 (numbering from the C-terminus). The equivalent sulphated tyrosyl residue in CCK-PZ is probably necessary for optimal activity of this polypeptide.5 The dose-response curves obtained by electrophysiological methods indicated that the relative potencies of the peptides on mouse pancreatic acinar cells were caerulein > CCK-PZ > gastrin. Synthetic human gastrin I was found to have a higher potency than either tetra- or pentagastrin.
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PMID:The effects of gastrin and gastrin analogues on pancreatic acinar cell membrane potential and resistance. 88 86

Both cholecystokinin (CCK-PZ) and gastrin stimulated antral rhythmic activity and raised fundal basal pressure. The antral motor effects were significantly blocked by pretreatment with atropine or tetrodotoxin. The fundal motor responses were almost unaffected. It is concluded that CCK-PZ and gastrin exert their antral motor effects essentially through local cholinergic neural pathways, while the motor responses in the fundus are almost entirely independent of these pathways.
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PMID:The role of local cholinergic pathways in the motor response to cholecystokinin and gastrin in isolated guinea-pig fundus and antrum. 92 15

1. Pancreatic volume flow as well as bicarbonate and protein secretion from pancreatic fistulas have been measured in response to i.v. infusion of graded doses of bombesin and related peptides containing the COOH-terminal fragment of the bombesin molecule in conscious dogs with intact antrum and in anaesthetized animals with antrectomy, or antrectomy and enterectomy. 2. Bombesin and related peptides given to conscious dogs produced a potent and dose-dependent increase in pancreatic protein output reaching a maximum equal to that induced by the octapeptide of cholecystokinin (OP-CCK) as well as a small rise in bicarbonate output attaining a peak amounting to about 10% of that evoked by secretin. The serum gastrin level rose progressively during the infusion of bombesin to reach a peak with the highest dose of peptide. 3. Bombesin infused i.v. in anaesthetized animals with resected antrum also evoked a marked increase in pancreatic protein secretion without significant changes in the serum gastrin level. Following the removal of the antrum and small intestine, bombesin failed to show any stimulation of the pancreatic secretion or any change in the serum gastrin level. It is concluded that the strong stimulatory action of bombesin and related peptides on pancreatic secretion cannot be entirely ascribed to the release of gastrin but might be attributed at least in part to the release of intestinal hormones, particularly CCK. 4. Atropine and the growth hormone-release inhibiting hormone (GH-RIH), which were shown to inhibit the release of CCK induced by duodenal perfusion of an amino acid mixture, also caused the inhibition of pancreatic protein secretion by bombesin but failed to affect the pancreatic response to OP-CCK. The results indicate that bombesin releases, in addition to gastrin, CCK from the gut by a mechanism largely dependent upon cholingeric innervation.
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PMID:Effect of bombesin and related peptides on the release and action of intestinal hormones on pancreatic secretion. 95 Jun 8


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