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)

A case with proteinlosing gastropathy with gastric hypersecretion of H+ and pepsin as well as hypergastrinemia is presented. Zollinger-Ellison syndrome was excluded by reduction in acid secretion and serum gastrin during the observation period as well as by the effect on gastric secretion and serum gastrin after injections of secretin and glucagon.
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PMID:Proteinlosing gastropathy with gastric hypersecretion of acid (H+) and pepsin and hypergastrinemia. A case report. 33 48

1. The effect of somatostatin and eighteen somatostatin analogues on pentagastrin-stimulated gastric acid and pepsin secretion was investigated in the conscious vagotomized cat prepared with chronic gastric fistulae. The majority of the analogues are peptides where D-amino acids are incorporated into the molecule instead of the natural L-isomers. 2. The ID50 for cyclic-somatostatin inhibition of near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 was found to be 1.29 +/- 0.13 n-mole kg-1 hr-1. Pentagastrin-stimulated pepsin secretion had a lower threshold to somatostatin inhibition than did acid secretion. 3. D-Phe6, D-Phe7, D-Thr10, D-Thr12 and D-Phe6-D-Trp8 analogues all show low biological activity against the secretion of gastric acid and pepsin, growth hormone, insulin and glucagon. None of these analogues are antagonists of the cyclic-somatostatin inhibition of gastric secretion, suggesting that they have low affinity for this somatostatin receptor. 4. The analogues under investigation show parallel changes in activity against gastric and growth hormone secretion, suggesting a similarity between the gastric and growth hormone receptors for somatostatin. 5. D-Cys14 analogues are equipotent with or have a greater potency than cyclic-simatostatin in inhibiting the secretion of gastric acid, growth hormone and glucagon but show low insulin inhibiting activity.
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PMID:Structure-activity relationships of eighteen somatostatin analogues on gastric secretion. 34 35

The role of cytosol components in the loss of rat liver adenylate cyclase activity which occurs during the preparation of particulate fractions from crude homogenates was studied. Epinephrine (5 micron)-, glucagon (10 micron)-, and fluoride (5 mM)- stimulated activities of twice-washed particulates were 31%, 58% and 67% of the homogenate activities, respectively. Addition of cytosol (100,000 X g supernatant devoid of adenylate cyclase activity) restored these activities to 82%, 88% and 80%. Cytosol also increased particulate basal activity from 60% of homogenate activity to 98%. The cytosol components capable of increasing adenylate cyclase activity were heat labile, nondialyzable, stable to freezing at -20 degrees, resistant to change of pH between 2 and 12, and unaffected by EGTA and NAD. Pretreatment with pepsin destroyed the effects of cytosol on both epinephrine- and glucagon-sensitive activities, whereas trypsin destroyed the effect of cytosol only on epinephrine-sensitive activity. The cytosol effect on adenylate cyclase was specific, since several purified proteins and ubiquitin, did not stimulate enzyme activity. Only part of the cytosol effect could be attributed to its GTP content. GTP at the concentration present in cytosol stimulated epinephrine-sensitive activity but significantly less than did cytosol, while GTP had no effect on glucagon-sensitive activity. Dialyzed cytosol retained its effectiveness even after removal of most (97%) of its GTP to a concentration where GTP had only a minimal effect on epinephrine-sensitive activity. Cytosol, unlike GTP, stimulated rather than inhibited activation by fluoride. Cytosol thus appears to contain at least two different protein components, which increase the activity of the two hormone-sensitive adenylate cyclases and presumably account in part for losses of adenylate cyclase activities seen during the preparation of particulates from homogenates.
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PMID:Activation of epinephrine and glucagon-sensitive adenylate cyclases of rat liver by cytosol protein factors. Role in loss of enzyme activities during preparation of particulate fractions, quantitation and partial characterization. 72 79

1. The peptic responses to Boots, GIH and synthetic secretins have been compared in fasting anaesthetized cats in which the pylorus and bile duct were occluded to prevent the release of duodenal hormones by acid and bile salts. A quantity of dilute acid introduced into the stomach at regular intervals ensured the total recovery of viscid secretions and preserved peptic activity. 2. The mean peak outputs of pepsin obtained in response to Boots secretin were significantly greater than the mean peak outputs of pepsin stimulated by equipotent doses of GIH secretin (4 Crick-Harper-Raper units of Boots secretin have been shown to stimulate a flow of juice and bicarbonate from the pancreas equal to that produced by 1 clinical unit of GIH secretin). The maximum output of pepsin stimulated by Boots secretin, 16 C.H.R. u./kg hr was 3 times the observed maximum output in response to the 4 times more potent dose of GIH secretin, 16 c.u./kg hr. The slopes of the log dose-response lines were significantly different for these two products indicating that their modes of action in stimulating pepsin may not be identical. 3. The outputs of pepsin following GIH and synthetic secretin were similar. Both these secretins stimulated the secretion of pepsin when infused in doses which stimulated the pancreas supramaximally. The less pure product Boots secretin evoked significantly higher peptic responses at doses submaximal for pancreatic stimulation, suggesting that a substance other than secretin exists in Boots preparations which contributes significantly to the overall output of pepsin in response to this product. The peptic response which was accompanied by a slight increase in acid output, but without any increase in pancreatic lipolytic activity, was not inhibited by atropine. This substance which is not present in highly purified GIH secretin does not appear to be cholic acid, gastrin, pancreozymin, glucagon or insulin. 4. The possibility that a vasodilator substance is present in Boots secretin which by expanding the splanchnic bed increases the concentration of secretin at target sites in the stomach and pancreas seems unlikely, as the flow of pancreatic juice does not increase proportionately with the vast increase in pepsin. A vasodilator substance which specifically affects the gastric vasculature remains a theoretical but unlikely explanation for our observation.
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PMID:A comparison of the pepsin stimulating effects of secretin preparations. 78 Dec 17

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

The effect of glucagon on gastric acid and pepsin secretion, basal or stimulated by a meal, pentagastrin and histamine, was studied in duodenal ulcer patients. Intravenous glucagon infused in graded doses ranging from 6.2 to 50 mug per kg-hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 40% of the control level at the dose of 50 mug per kg-hr. Acid inhibition was paralleled by a decrease in the pepsin output and serum calcium level and was accompanied by a rise in the blood glucose concentration. Glucagon used in a standard dose of 25 mug per kg-hr produced about 50% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in the serum gastrin level measured by radioimmunoassay. Histamine-induced secretion was only slightly inhibited by glucagon, and the degree of inhibition for acid (25%) and pepsin (20%) secretion was statistically insignificant.
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PMID:Effect of glucagon on meal-induced gastric secretion in man. 108 77

Protein carboxyl methyltransferases from erythrocytes and brain appear to catalyze the esterification of L-isoaspartyl and/or D-aspartyl residues but not of normal L-aspartyl residues. In order to identify the origin of these unusual residues which occur in subpopulations of a variety of cellular proteins, we studied the in vitro methylation by the erythrocyte enzyme of glucagon, a peptide hormone of 29 amino acids containing 3 aspartyl residues and a single asparagine residue. Methylated glucagon was digested with either trypsin, chymotrypsin, pepsin, or endoproteinase Arg C, and the labeled fragments were separated by high-performance liquid chromatography and identified. In separate experiments, methyl acceptor sites were determined by digesting glucagon first with proteases and then assaying purified glucagon fragments for methyl acceptor activity. Using both approaches, we found that the major site of methylation, accounting for about 62% of the total, was at the position of Asp-9. Chemical analysis of fragments containing this residue indicated that this site represents an L-isoaspartyl residue. A second site of methylation, representing about 23% of the total, was detected at the position of Asn-28 and was also shown to represent an L-isoaspartyl residue. Methyl acceptor sites were not detected at the positions of Asp-15 or Asp-21. Preincubation of glucagon under basic conditions (0.1 M NH4OH, 3 h, 37 degrees C) increased methylation at the Asn-28 site by 4-8-fold while methylation at the Asp-9 site remained unchanged. These results suggest that methylation sites can originate from both aspartyl and asparaginyl residues and that these sites may be distinguished by the effect of base treatment.
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PMID:Methylation at specific altered aspartyl and asparaginyl residues in glucagon by the erythrocyte protein carboxyl methyltransferase. 359 86

After various types of sympathectomy (surgical, chemical, isolated adrenodemedullation; AMX, combined procedures) in the rat, basal gastric secretion, gastric mucosal blood flow (MBF), associated glucose and a variety of hormones in the blood were measured. With the exception of the ineffective surgical sympathectomy, all the other forms variously influence gastric secretion qualitatively (volume, acidity, pepsin) and quantitatively (output per unit time). Chemical sympathectomy has an augmenting effect both on acid (volume, acidity, output) and on pepsin. In general the MBF parallels acid, but the MBF is decreased after AMX despite stable or increased gastric secretion. Sympathectomy, except procedures involving AMX or AMX + surgical sympathectomy, increases spontaneous gastric mucosal lesions. With AMX glucose is diminished, but is elevated following surgical and chemical sympathectomy. Gastrin, insulin and somatostatin are always higher than in sham-operated controls, glucagon after surgical sympathectomy only. It is concluded that (1) the sympathoadrenal system in the rat modulates both basal gastric secretion and blood hormones; (2) the adrenal medulla may participate in the control of gastric MBF, and (3) gastric mucosal lesions are not correctly reflected by the ration MBF/acidity.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of sympathectomy. 612 14

After vagotomy (truncal, highly selective, superselective) in rats, basal gastric secretion, gastric mucosal blood flow, associated fasting blood glucose and a variety of hormones were measured. All forms of vagotomy reduce acid (volume, acidity, output), but highly selective and superselective--though not truncal--procedures stimulate basal pepsin secretion, whereas mucosal blood flow roughly parallels acid production. Spontaneous gastric mucosal lesions increase after highly selective vagotomy. Both highly selective and superselective--but not truncal--vagotomy tend to increase plasma glucose and somatostatin, while only the former reduces insulin and glucagon. Common to all vagotomies is the development of virtually undetectable calcitonin (less than 25 pg/ml) and of hypergastrinemia. It is concluded that in the rat with draining gastric fistula in response to vagotomy there are moderate differences in regard to gastric mucosal ulcer index, gastric secretion, glucose, glucose-regulating hormones, while lowered calcitonin may be a general feature of low vagal tone.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of vagotomy. 612 15

Hanisch E, Schwille PO. Effects of various vagotomies and sympathectomies on gastric secretory function in the non-stressed and by immobilization stressed rat. Scand J Gastroenterol 1984, 19, Suppl 89, 99-104 The aim of the present study was to study several gastrointestinal parameters (acid, pepsin secretion, ulcer index, gastrin, somatostatin, glucagon) following various forms of sympathectomies in comparison with vagotomies under two different states of sympatho-adrenal activation in male gastric fistula rats. It is concluded that acid and pepsin appear regulated by the autonomous nervous system, even in the basal state. Gastric ulcer formation/prevention depends on gastric sympathetic innervation and on the state of activation of the adrenal medulla. Basal gastrin, somatostatin, glucagon may be modified by both limbs of the autonomous nervous system.
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PMID:Effects of various vagotomies and sympathectomies on gastric secretory functions in the non-stressed and by immobilization stressed rat. 614 96


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