Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unspecific binding of immunoglobulins to gastrin, somatostain and glucagon cells of the gastrointestinal mucosa or pancreas has been found to occur through a nonantigen-antibody mechanism mediated by the C14 fraction of complement. The phenomenon represents an important drawback in hormone immunohistochemistry, which can be overcome by using complement deprived, highly dilute anti-hormone sera.
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PMID:Complement-mediated binding of immunoglobulins to some endocrine cells of the pancreas and gut. 47 71

The inhibitory effects of intravenous infusions of secretin, glucagon and caerulein on the gastric acid response to bombesin were studied in 8 duodenal ulcer patients. Bombesin was found to be a very potent stimulator of gastric acid secretion in patients with duodenal ulcer. There were no significant differences in acid outputs per 15-min period between bombesin infused in a dose of 0.9 microgram/kg/h and pentagastrin infusion administered in a maximal dose, at a rate of 6.0 microgram/kg/h. Secretin (1 U/kg/h), glucagon (30 microgram/kg/h) and caerulein (0.1 microgram/kg/h) produced significant decreases in gastric acid secretion evoked by bombesin given in a dose of 0.9 microgram/kg/h. Percentages of inhibition were 48.6, 45.2 and 35.5, respectively. It is supposed that secretin and glucagon given in pharmacological doses are capable of interfering with the action of gastrin released from antrum by means of bombesin on the parietal cell by noncompetitive kinetics. Caerulein administered in a pharmacological dosis, however, can inhibit the effect of gastrin released by bombesin on the parietal cells by a competitive kinetic.
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PMID:Inhibition of bombesin-stimulated gastric acid secretion by secretin, glucagon and caerulein in patients with duodenal ulcer. 48 52

Fasting serum gastrin, cholecystokinin, glucagon, and gastric inhibitory polypeptide concentrations were simultaneously measured in normal subjects and in patients with different degrees of renal failure. Values of gastrin, cholecystokinin, gastric inhibitory polypeptide, and glucagon were significantly higher in all patients with serum creatinine concentrations greater than 3 mg/dl than in controls (P less than 0.01). The degree of renal insufficiency was significantly correlated (P less than 0.05) with serum concentrations of each hormone, but no significant linear correlation existed among the serum concentrations of different gastrointestinal hormones in individuals. Hemodialysis did not significantly alter predialysis serum gastrin, cholecystokinin, or glucagon concentration, but the serum gastric inhibitory polypeptide concentration decreased by 30% (P less than 0.01) after hemodialysis. The disproportionate increases of hormones with antagonistic actions may alter gastrointestinal function in renal insufficiency.
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PMID:Gastrointestinal hormone profile in renal insufficiency. 51 44

The blood serum levels of gastrin and insulin and arterial blood levels of glucose were determined immediately before intravenous injection of 1 mg of glucagon, and 10, 20, 40 and 60 minutes later in 12 gastric ulcer patients, 14 duodenal ulcer patients and 12 controls using the radioimmunological and orthotoluidine methods respectively. Following glucagon administration the gastrin levels dropped in the controls and the gastrin patients, and increased in the duodenal patients by an average of 30%. Insulin levels increased in all three groups, but the increase was statistically significant in the two patients groups. Glucose levels in the blood also increased with no significant differences between the groups. It is suggested that the different effect of glucagon on gastrin levels may be due to gastrin-insulin interaction; the levels of the two hormones in the blood of duodenal patients were higher than in the other two groups studied.
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PMID:The effect of glucagon on the blood levels of gastrin, insulin and glucose in patients with gastric and duodenal ulcers. 52 17

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

Hypersecretion of gastric acid and accelerated intestinal transit are largely unexplained consequences of massive resection of the small bowel; several postulated humoral mechanisms remain unsubstantiated. The purpose of the study was to investigate the effects of 75% resection of the distal small bowel in dogs on circulating levels of a range of gastrointestinal hormones. Basal and meal-stimulated concentrations of insulin, secretin, gastrin, pancreatic glucagon, and total glucagon-like immunoreactivity (GLI) were measured by radioimmunoassay techniques. After resection, significant depletions of basal and stimulated total GLI (p less than 0.05 -- p less than 0.001) and a significant rise of stimulated gastrin (p less than 0.05) were discovered. These hormonal alterations may produce an important imbalance of humoral influences on gastrointestinal function. It is suggested that these changes may hold a key to the aetiology of the complications of massive resection of the small bowel.
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PMID:Role of gastrointestinal hormones in the response to massive resection of the small bowel. 59 Aug 47

The aim of the present study was to investigate the effect of somatostatin (growth-hormone release-inhibiting hormone) on ulcer formation during immobilisation stress. This was done in male Albino-rats to study the effect of somatostatin on number and size of ulcers, to calculate ulcer index, to measure pH-value of gastric juice as well as plasma levels of gastrointestinal hormones. Rats treated with somatostatin before and during stress exposition had only the third part of the ulcers compared with the untreated animals. Total ulceration area was less than the tenth of the untreated rats. Normal corticoid plasma levels during stress exposition were found in the lower range of normal values in somatostatin treated rats. Decrease of plasma gastrin during stress exposition exceeded the gastrin decrease of somatostatin treated rats. Rise of plasma glucagon was completely inhibited during somatostatin application. Results of serum glucose paralleled those seen in glucagon.
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PMID:Prophylactic effect of somatostatin on stress ulcer formation in rats. 60 21

An experimental study was conducted on the effect of resection of the jejunum and ileum on gastrin release. The intravenous infusion of L. arginine in a dose of 0.5 g per kg body weight for 30 minutes proved to be most practical in evaluating gastrin release in addition to insulin and glucagon release. Serum gastrin levels in response to this dose of arginine were determined before and three weeks, three months and one year after resection of the jejunum and of the ileum. At three weeks, a significant increase in gastrin levels occurred in bothe the fasting state and after stimulation in dogs with either jejunum or ileum resection. At three months, the elevated gastrin response persisted only in those with jejunum resection. By one year, the gastrin levels had fallen in almost all dogs to approximately the preoperative levels.
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PMID:Follow-up study of gastrin response after resection of the jejunum and the ileum. 60 74

Ileocecal shincter (ICS) pressure was evaluated in response to hormonal and pharmacological stimuli in rabbits. The effect of exogeneous gastrin (pentagastrin) and glucagon, metoclopramide and neostigmin on the ICS pressure was studied. Gastrin, glucagon and metoclopramide increased the pressure whereas neostigmin lowered it. These results suggest that this junctional zone is not only a valve but a real shincter, which is affected by gastrointestinal hormones and pharmacological substances. Further examinations are necessary to study the role of the ICS after gastrointestinal surgery.
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PMID:[Hormonal and pharmacological modification of the ileocecal sphincter]. 61 12

Dispersed mucosal cells (approx. 70% parietal cells) prepared from guinea pig stomach maintained their cellular concentration of potassium (65--80 nmol potassium/10(6) cells) for at least 5 h in vitro. Uptake of 42K by dispersed gastric mucosal cells depended on temperature, H+ concentration and oxidative metabolism. Carbachol and, in some instances, gastrin caused a 40--50% increase in cellular uptake of 42K as a consequence of the ability of these agents to increase 42K influx. Ouabain reduced uptake of 42K by 70% but did not alter the effect of carbachol. Cellular uptake of 42K was not altered by histamine, prostaglandin, E1, glucagon, secretin, vasoactive intestinal peptide or C-terminal octapeptide of cholecystokinin. Uptake of 42K was also increased by dibutyryl cyclic AMP or dibutyryl cyclic GMP but not by cyclic AMP, cyclic GMP or their 8-bromo derivatives. Theophylline caused a small (10--15%) increase in 42K uptake and potentiated the increase caused by submaximal concentrations of carbachol. The increase in 42K uptake caused by either dibutyryl cyclic nucleotide and carbachol was additive.
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PMID:Potassium transport in dispersed mucosal cells from guinea pig stomach. 63 44


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