Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral (50 mg/ml) or central (50 micrograms/microliter) injections of proglumide were made into Sprague-Dawley rats which displayed satiety-like responses after the peripheral (100 micrograms/kg) or central (50 ng in 1 microliter) administration of cholecystokinin (CCK). The satiety produced by CCK injection into the lateral hypothalamus, area postraema and ventromedial hypothalamus was significantly reversed by proglumide injections into these areas during a 4 h food intake test. Peripheral injection of proglumide after central or peripheral CCK injection did not modify this type of CCK-induced satiety. Central proglumide injection produced a reliable decrease in water intake and this is compatible with previous findings which describe the stimulation of water intake after central gastrin administration. These results suggest that various central and peripheral mechanisms which are involved in the regulation of appetite may function independently as a 'failsafe' system.
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PMID:Central and peripheral proglumide administration and cholecystokinin-induced satiety. 353 20

The molecular species of gastrin in the circulation and in tumor extracts were studied in two groups of patients: (1) with benign gastrinoma and (2) with gastrinoma with liver metastases. Radioimmunoassays (RIAs) and immunoaffinity chromatography for the amino (NH2)- and amidated COOH-terminus of gastrin-17 (antiserum G17) and the NH2-terminus of gastrin-34 (antiserum G34) were employed. In both benign and metastatic tumors the molecular forms of gastrin in boiling water extracts measured by the gastrin-17 NH2- and COOH-terminal assays were similar. In addition to a molecular component resembling the amidated gastrin-17, there were also significant amounts of larger molecular weight (mol. wt.) forms. The larger mol. wt. forms absorbed by the NH2-terminus of G17 antiserum corresponded to the COOH-terminus-extended forms of gastrin-17. Furthermore, larger mol. wt. gastrins immunopurified by antiserum to the NH2-terminus of gastrin-34 corresponded to gastrin-34 extended molecules. Sera of patients with liver metastases had higher concentrations of the NH2-terminal of gastrin-17 whereas sera of patients with benign gastrinoma contained predominantly gastrins detected by the COOH-terminal assay. These results suggest that: (a) there are differences in the molecular pattern of gastrin in the circulation of patients with benign and metastatic gastrinomas; (b) gastrins which are fully processed with carboxy-terminal amidation predominate in the circulation of patients with benign gastrinoma; and (c) gastrins containing the gastrin-17 and COOH-terminally extended gastrin-17 and gastrin-34 precursor molecules occur in high concentration in the circulation of gastrinoma patients with metastases to the liver.
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PMID:Identification of gastrin molecular variants in gastrinoma syndrome. 355 1

Little is known of the identity of gastrin/cholecystokinin (CCK)-like peptides in protochordates. These animals are at a level of organization corresponding to that from which the vertebrate line arose; in order to shed light on the origins of gastrin/CCK-like peptides, we have studied by immunochemical methods these peptides in a protochordate, Ciona intestinalis. In radioimmunoassay, boiling water extracts of the neural ganglion reacted with C-terminal specific gastrin/CCK antibodies, but not N-terminal or intact G17 specific antibodies. Of particular importance was the fact that a gastrin antibody which reacts weakly with CCK8 showed full activity with the Ciona material, suggesting that it resembles the C-terminus of gastrin. A single major peak was found by gel filtration and HPLC. In immunohistochemistry, nerve cell bodies were found in the cortical regions of the ganglion, and abundant fibres ramified in the central neuropile. We conclude that peptides of the gastrin/CCK series occur in nervous tissue in protochordates, and that while they are distinguishable from known forms of both gastrin and CCK, they resemble C-terminal fragments of the mammalian gastrins.
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PMID:Identification and localization of material with gastrin-like immunoreactivity in the neural ganglion of a protochordate, Ciona intestinalis. 356 99

The effects of coffee on exocrine pancreatic secretion are unknown but may be important, because a link between chronic stimulation of pancreatic secretion and experimental chemical carcinogenesis and an association between coffee drinking and human pancreatic adenocarcinoma have been reported. We measured exocrine pancreatic trypsin and gastric acid secretions collected through orogastroduodenal tubes and serum gastrin in eight non-coffee drinkers and eight coffee drinkers. During fasting, after one interdigestive cycle control period, one of four 250-ml samples [plain water, water plus caffeine (4.6 mg/kg), decaffeinated coffee (127.9 mg/kg), caffeinated coffee (127.9 mg/kg)] was administered through the orogastric tube. Caffeinated and decaffeinated coffee (p = 0.008), caffeine (p = 0.03), and an unidentified substance(s) in coffee other than caffeine (p = 0.008) were associated with increased interdigestive exocrine pancreatic trypsin secretion. In addition, we also confirmed that coffee and caffeine stimulated gastric acid secretion (p = 0.02) and decaffeinated coffee raised serum gastrin concentrations (p = 0.005). If an association between coffee and pancreatic carcinogenesis exists, chronic stimulation of the exocrine pancreas by secretagogues could result in a gland susceptible to carcinogenesis.
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PMID:The acute effects of coffee and caffeine on human interdigestive exocrine pancreatic secretion. 357

The effects of three types of white wine (10% ethanol; pH 2.84-3.26), Coke (pH 2.45) and water (pH 8.03) on basal and food-stimulated gastric acid secretion in dogs were investigated. Water and Coke did not significantly modify acid secretion and gastrin release under basal conditions. By contrast, white wine or water +10% ethanol significantly increased acid secretion, with a tendency to elevate plasma gastrin concentrations. Acid secretion and gastrin release induced by a standard meal were not significantly modified by previous administration of Coke and water. In contrast, white wine and water +10% ethanol significantly increased food-stimulated total acid output, without changing plasma gastrin levels. It is concluded that Coke and water have only trivial effects on basal and on food-stimulated gastric acid secretion and gastrin release in the dog. The gastric stimulant effect of white wine is mainly related to its percentage of alcohol regardless of the slight differences in pH of the solutions.
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PMID:Effects of white wine, Coke and water on basal and food-stimulated gastric acid secretion and gastrin release in the dog. 366 12

Cholecystokinin (CCK) is a heterogeneous gut hormone which is also synthetized in extra-intestinal endocrine cells and neurons. In order to examine the possibility that CCK peptides are local modulators of calcitonin secretion, we have studied the structure-activity relationship on calcitonin secretion from perfused canine thyroid lobes as well as the presence and molecular nature of CCK in the thyroid. Peptides containing the intact COOH-terminal tetrapeptide amide of CCK (CCK-4, CCK-5, pentagastrin, CCK-8 and gastrin-17) all induced dose-dependent (0.1, 3 and 100 nmol/l) increases in calcitonin release (P less than 0.05, n = 4) with biphasic secretion during 6-min infusion periods. The deamidated tetrapeptide and the COOH-terminal tripeptide were without effect. Gel chromatography of neutral water and acid-ethanol extracts of thyroid tissue, monitored by sequence-specific CCK and gastrin radioimmunoassays, disclosed a variety of CCK and gastrin peptides of which a predominant form resembled small molecular forms like CCK-4 and CCK-5. The presence in the thyroid of small CCK-like peptides and the pronounced effect of such peptides on calcitonin secretion suggest that calcitonin secretion is modulated by local release of small CCK peptides. They could originate from intrathyroidal nerves or from sub-populations of C-cells.
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PMID:Cholecystokinin peptides as local modulators of thyroidal calcitonin secretion in the dog? 366 49

We evaluated the hypothesis that the noncaffeine gastric acid stimulant effect of coffee might be by way of serum gastrin release. After 10 healthy volunteers drank 50 ml of coffee solution corresponding to one cup of home-made regular coffee containing 10 g of sugar and 240 mg/100 ml of caffeine, serum total gastrin levels peaked at 10 min and returned to basal values within 30 min; the response was of little significance (1.24 times the median basal value). Drinking 100 ml of sugared water (as control) resulted in occasional random elevations of serum gastrin which were not statistically significant. Drinking 100 ml of regular or decaffeinated coffee resulted in a prompt and lasting elevation of total gastrin; mean integrated outputs after regular or decaffeinated coffee were, respectively, 2.3 and 1.7 times the values in the control test. Regular and decaffeinated coffees share a strong gastrin-releasing property. Neither distension, osmolarity, calcium, nor amino acid content of the coffee solution can account for this property, which should be ascribed to some other unidentified ingredient. This property is at least partially lost during the process of caffeine removal.
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PMID:Effect of regular and decaffeinated coffee on serum gastrin levels. 374 48

Cholecystokinin octapeptide (CCK-8), administered intracerebroventricularly (i.c.v.), will suppress feeding. The aim of the present study was to determine the pharmacological characteristics of this satiety inducing effect in rats. For this purpose, we employed a feeding bioassay model in 24 h fasted rats and examined the effects of CCK-8 and a variety of structurally related analogs on latency to feed after i.c.v. injection and on the amount of food and water consumed as measured after the initiation of feeding in sequential 20-min epochs for 1 h. CCK-8, given in doses of 0.1, 1 and 10 nmol, produced a dose-dependent increase in feeding latency and a reduction of food intake during the first 20 min after initiation of feeding. Food intake during the next 40 min and water consumption were not altered. Plasma levels of CCK-like immunoreactivity after an i.c.v. injection of a dose of CCK-8 which blocked feeding (10 nmol) rose insignificantly from 117 to 125 pg/ml. In contrast, at the minimally effective dose of CCK-8 after i.v. administration (10 nmol), which also produced an inhibition of feeding, the plasma level was 1430 pg/ml. This difference indicates that plasma levels of CCK after i.c.v. CCK-8 are not adequate to produce the observed feeding suppression and suggests that the effects of i.c.v. CCK-8 are not mediated by a peripheral redistribution. Systematic dose response studies revealed the following rank order of potencies: CCK-8 greater than or equal to G-17 II much greater than CCK-8 NS = G-17 I greater than or equal to CCK-4 = CCK 26-29 = 0. Only gastrin-17 II (sulfated) produced an effect comparably significant to CCK-8. I.c.v. proglumide at 2500 nmol failed to modify the effects of CCK-8 at 10 nmol after i.c.v. injection. These data demonstrate that the structural requirements for feeding suppressive activity in rat brain are the carboxyterminus with a sulfated tyrosine residue, located 6 to 7 residues from the carboxyterminus, as present in CCK-8 and gastrin-17 II.
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PMID:Intracerebroventricular injections of cholecystokinin octapeptide suppress feeding in rats--pharmacological characterization of this action. 374 26

The effects of mild heat exposure (30 degrees C; 30% relative humidity), and of the suppression of prolactin secretion under such conditions, were studied in anoestrous ewes given daily 791 g dry matter of a pelleted mixture of lucerne hay and oat grain (3:2). 51Cr-EDTA, 103Ru-phenanthroline and lignin were used to determine mean retention times (MRT) in the gastro-intestinal (GI) tract by a continuous infusion-total sampling procedure. Mild heat exposure reduced the digesta-free tissue weight of all GI tract segments distal to the omasum. Increases in the amounts of digesta in the stomach compartments were largely due to increases in water content, although the solids content of the abomasum (P less than 0.10) and omasum also increased. The treatment caused an increase in water intake (P less than 0.10), increased the MRT of 51Cr-EDTA in the reticulo-rumen (P less than 0.05), and tended to increase the MRT of all three markers in the omasum and abomasum. However, MRT in the whole GI tract was unaffected because of a compensating decrease (P less than 0.01) in digesta MRT in the distal large intestine. Suppression of prolactin secretion with 2-bromo-alpha-ergocryptine impaired the ewes' ability to maintain their body temperature under the warm conditions imposed. This was associated with a consistent reduction in the degree to which water intake and its transactions in the GI tract changed in response to mild heat exposure. The treatment also caused decreases in omasal MRT and increases in abomasal MRT. Increased plasma concentrations of somatostatin and gastrin were associated with reduced plasma concentrations of prolactin, and it was postulated that some of the effects of prolactin on the GI tract may be mediated via somatostatin.
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PMID:Effects of mild heat exposure and suppression of prolactin secretion on gastro-intestinal tract function and temperature regulation in sheep. 377 61

Using an antiserum generated against synthetic CCK-10, we have developed a radioimmunoassay specific for the carboxyl-terminus of cholecystokinin (CCK). Three rabbits were immunized with synthetic sulfated carboxy-terminal CCK decapeptide (CCK-10) conjugated to keyhole limpet hemocyanin. Using 125I-CCK-39 prepared by the Iodogen method as a tracer, we found that all immunized rabbits produced antibodies against the conjugate. Antiserum R016 had the highest titer (1:225,000 after four immunizations) and was studied most extensively. R016 recognizes all molecular forms of CCK, including unsulfated and oxidized forms, but has negligible cross-reactivity with gastrin and other peptides. Using CCK-8 as a standard, the assay has a minimum detection limit of 0.5 pM and an ED50 of 11.5 pM. Serial dilutions of water/acid extracts of canine intestine were parallel to serial dilutions of sulfated CCK-8, CCK-33 and CCK-39. The assay was used to measure CCK concentrations in canine plasma after C18 Sep-Pak extraction; the concentration of immunoreactive CCK increased from a basal value of 7.8 +/- 1.0 to 9.5 +/- 1.2 and 11.1 +/- 1.2 pM 30 and 60 min postprandially (P less than 0.05 by paired analysis). This sensitive and uniquely specific CCK radioimmunoassay should be useful in characterizing several aspects of CCK physiology and the method for generating CCK antisera should be of value to other investigators.
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PMID:Development of cholecystokinin radioimmunoassay using synthetic CCK-10 as immunogen. 378 38


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