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)

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

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

Caerulein is a dekapeptide related to gastrin and cholecystokinin with profound effects on gastrointestinal motility. In the present study we examined the effect of intravenously administered caerulein (0.1 microgram/kg body weight) on the intraluminal pressure of common bile duct and duodenum in 12 patients. The pressure recordings were obtained by endoscopic perfusion manometry. The tip of the perfused catheter was positioned under radiological control and the measurements were carried out under standardized conditions. Following the injection of caerulein there was a rise in pressure in the common bile duct and the mid portion of the duodenum. The pressure increase in the common duct appears to be predominantly due to contraction of the gallbladder as it is considerably less pronounced in patients with cholecystectomy. The problems inherent to endoscopic pressure recordings under pharmacological stimulation are discussed.
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PMID:[The effect of caerulein on intraluminal pressures of the common bile duct and duodenum in man (author's transl)]. 90 6

In rats given a copper-deficient diet plus penicillamine to destroy the acinar tissue selectively, the sensitivity and secretory pattern of pancreatic duct cells to a variety of hormones has been investigated. Resting flow rate of this pancreatic duct model was in the same range as in the intact gland. The duct cells responded to increasing doses of secretin by producing more juice with increasing outputs of bicarbonate, sodium, potassium, and chloride. Bicarbonate concentration increased with the lowest dose of secretin up to values of 64 mEq per liter and did not further increase with higher doses of secretin and increasing secretory rates. The concentration of potassium increased with increasing doses of secretin and flow rates, whereas chloride concentration decreased in a reciprocal fashion to bicarbonate. Gastrin and cholecystokinin-pancreozymin did not significantly stimulate the duct cells. Atropine did not inhibit the action of secretin on the flow rate or on bicarbonate secretion.
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PMID:Pancreatic duct cells in rats: secretory studies in response to secretin, cholecystokinin-pancreozymin, and gastrin in vivo. 90 83

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a concentration of 25 ng/ml produced a prompt, but transient statistically significant, twofold rise in mean somatostatin concentration. Secretion at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two- to threefold rise in mean somatostatin release, which persisted throughout the perfusion period. With all four polypeptides the pattern of the somatostatin response resembled that of insulin. It appears that pancreatic somatostatin release is stimulated by gastrointestinal hormones that influence the secretion of insulin and glucagon.
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PMID:The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas. 90 61

A number of gastrin antisera, which in radioimmunoassay systems showed no or negligible cross-reactivity towards the structurally and functionally related peptide cholecystokinin were found to react with both gastrin and cholecystokinin cells when used for immunocytochemistry. This discrepancy was shown to be due either to reactivity against a COOH-terminal region common to gastrin and cholecystokinin or to the occurrence of heterogenous antibody populations in the antisera. By differential absorptions the latter type of antisera could be rendered specific for gastrin. Antisera reactive against the NH2-terminal, middle or COOH-terminal regions of human heptadecapeptide gastrin were prepared and together with a specific cholecystokinin antiserum used for the characterization of antral gastrin cells of different species. The results indicate that only the COOH-terminal region of gastrin is conserved during evolution.
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PMID:Characterization of antral gastrin cells with region-specific antisera. 92 41

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

The pressure-volume (PV) response of the opossum gallbladder was studied under basal conditions and after the continuous intravenous infusion of gastrin I, secretin, and cholecystokinin (CCK). The hormone effects were examined individually and in combination. The unstimulated gallbladder was capable of accommodating increases in intraluminal volume with only slight changes in intraluminal pressure. Cholecystokinin significantly increased the pressure recorded from the gallbladder. The pressure generated depended on the concentration of CCK and the intraluminal volume. Gastrin I had no independent effect on the PV response of the gallbladder but reduced the stimulatory affect of CCK. Secretin, alone, decreased the PV response of the gallbladder. Secretin also antagonized the stimulatory response to CCK. These findings suggest that the regulation of gallbaldder motor function and pressure generation exclusive of neural input, may depend on the interaction of CCK with gastrin and secretin and the intraluminal volume of the organ at the time of stimulation.
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PMID:Gallbladder pressure-volume response to gastrointestinal hormones. 93 33

The total concentration of gastrin and distribution of gastrin components were examined in mucosal biopsies from corpus, antrum, duodenum, and jejunum from normal subjects and patients with duodenal ulcer. The concentration was highest in the antrum, being 12.1+/-1.9 nmol per g of mucosa (mean +/-SEM) for normal subjects, and 9.0 +/-1.6 nmol per g of mucosa for duodenal ulcer patients (P eaual to 0.03). A steep gradient was found distally: in the proximal duodenum the concentration was 0.1; in the distal duodenum, 0.02 to 0.01; and in the proximal jejunum, less than 0.01 of the antral concentration. In corpus of the stomach, the concentrations were similar to those found in the jejunum. Gel filtrations showed that most gastrin immunoreactivity was eluted in positions corresponding to serum component II (gastrin-34-like) and III (gastrin-17-like), but immunoreactivity corresponding to all the components present in serum was found. No interference from cholecystokinin was observed in duodenal biopsies. In corpus, antrum, and jejunum component III was the predominant form, whereas component II made up half of immunoreactive gastrin in the duodenum. No major differences were observed between normal subjects and duodenal ulcer patients. There was no simple relationship between acid secretion and mucosal gastrin concentration, but ulcer patients with the highest acid secretion had the lowest antral content and the highest duodenal content.
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PMID:Gastrins in tissue. Concentration and component pattern in gastric, duodenal, and jejunal mucosa of normal human subjects and patients with duodenal ulcer. 94 52

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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