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)

This is a review of current information concerning the role of hormones and the autonomic nervous system in the control of exocrine secretions of the pancreas. A greater emphasis has been placed on the role of hormones because of information accumulated during the last several years. With the development of radioimmunoassay techniques, it is now possible to correlate circulating hormone concentrations with biological function. The role of hormones has been discussed with the framework of the secretin-glucagon family, the cholecystokinin-gastrin family, and other proposed gastrointestinal hormones and related peptides. Gastrin, secretin and cholecystokinin-pancreozymin are three prime gut hormones that regulate pancreatic secretion. Other hormones that may have a role in pancreatic secretion include glucagon, vasoactive intestinal polypeptide, chymodenin, somatostatin, pancreatic polypeptide, motilin, and bombesin. Neural mechanisms play an important although not so succinct a role in the over-all control of exocrine secretion. A complex relationship exists between the parasympathetic nervous system and the release of the hormones and their effect on pancreatic acinar and duct cells.
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PMID:Neurohormonal control of pancreatic secretion. A review. 34 Mar 22

Residual beta cell function was studied in 18 juvenile-onset diabetics by measuring serum C-peptide immunoreactivity (CPR) fasting, and after IV injection of glucagon (1 mg). This was compared with the exocrine pancreatic response to an IV infusion of secretin and cholecystokinin-pancreozymin. Outputs of pancreatic bicarbonate, amylase and trypsin were measured. Exocrine secretory pancreatic function was decreased in 14 patients. Fasting and maximal CPR showed that 9 patients had residual insulin secretion. For these 'CPR-secretors' there was a strong correlation between CPR and output of bicarbonate (r = 0.87, p less than 0.005) and amylase (r = 0.7, p less than 0.05), but not with trypsin. These results suggest the existence of an endocrine-exocrine relationship in the pancreas.
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PMID:The effect of residual insulin secretion on exocrine pancreatic function in juvenile-onset diabetes mellitus. 34 40

Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
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PMID:The effect of glucagon on the exocrine pancreas. A review. 36 5

A 45-year-old man was operated for surgical treatment of a long-standing peptic ulcer disease and upon inspection of the pancreas for suspected Zollinger-Ellison syndrome, tumor nodules were found in this organ. The tumor tissue examined by immunofluorescence showed specific staining only after incubation with anti-pancreatic polypeptide. Negative results were obtained with antisera directed against insulin, pancreatic glucagon, somatostatin, GLI, VIP, secretin, and gastrin. Examination of the tissue by electron microscopy revealed a homogeneous population of small granule-containing cells. This case, therefore, illustrates a tumor composed of one single hormone-producing cell type and allows definition of the ultrastructural features of human pancreatic polypeptide-containing cells.
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PMID:Human islet cell tumor storing pancreatic polypeptide: a light and electron microscopic study. 37 22

To examine gut-islet interrelationships, we entirely separated the gastrointestinal tract from the rat. When we arterially perfused this preparation with an erythrocyte-free solution for 1 h, it remained histologically intact and took up oxygen and glucose. Feedings were given via a duodenal tube. The gut absorbed glucose when glucose in the feeding was high (9.2 g/dl), but not when glucose in the feeding was low (58 mg/dl). With feeding, the portal venous effluent (PVE) from this preparation (stomach to ileum) enhanced late-phase, glucose-induced insulin secretion from pancreas of another rat. This enhancement occurred when the gut was fed either glucose (9.2 g/dl) in electrolyte solution or electrolyte solution alone. PVE from glucose-fed upper gut (stomach, duodenum) was similarly insulinotropic. In contrast, PVE from unfed gut or from glucose-fed gut of old rats was not insulinotropic. PVE from all gut preparations except upper gut produced a glucagon "spike" during basal pancreatic perfusion. Effects of gastrointestinal peptides (gastric inhibitory polypeptide, cholecystokinin octapeptide, secretin, gastrin) and immunoassays of PVE suggested that the insulinotropic substance is not one of these peptides. Thus, an insulinotropic substance that is not dependent on feeding nutrient material is secreted from the intestine.
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PMID:Secretion of an insulinotropic factor from isolated, perfused rat intestine. 37 52

Peptides identical or related to mammalian gut hormones occur widely, not just in gut endocrine cells but also in central or peripheral nerves, amphibian skin glands, and a variety of invertebrate tissues. The dual distribution in brain and gut was probably already established early in the vertebrate line; representatives of the oldest vertebrate group, the cyclostomes, have cholecystokinin-like factors in gut endocrine cells and in brain. The related sequences of certain gut peptides, notably gastrin and cholecystokinin (CCK), and secretin, glucagon, vasoactive intestinal polypeptide (VIP), and gastric inhibitory peptide (GIP), indicate evolution from common ancestral molecules by gene duplication and divergence. Functionally important residues are conserved. Thus the COOH-terminal pentapeptide common to gastrin and CCK also contains their minimal active fragment. There are also evolutionary changes at the level of the target organ receptor mechanisms: these are also evolutionary changes at the level of the target organ receptor mechanisms; these are illustrated by evidence suggesting that secretin regulates the flow of pancreatic juice in mammals whereas the structurally related peptide VIP has a similar role in birds.
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PMID:Evolutionary relationships of the gut hormones. 37 11

A 58-year-old patient with hypergastrinemia (basal and after stimulation by means of protein food, calcium, glucagon, and secretin), acid hypersecretion, recurrent anastomotic ulcer, gastrocolonic fistula, steatorrhea, and malabsortion (hypocalcemia, hypocholesterolemia and a rather elevated 5-HIAA) is reported. The definite preoperative diagnosis of Zollinger-Ellison syndrome was established after the intravenous secretin test (75 U) which produced a significant stimulation peak 5 minutes after being injected. The possible existence of a multiple endocrine adenomatosis syndrome type I was discarded. During the operation no pancreatic or extrapancreatic macroscopic tumor was found. A total gastrectomy, transverse colectomy, splenectomy, and subtotal pancreatic resection were performed; Rosanow's techniques was used to re-established the gastrointestinal continuity. The morphological study of the excised pancreatic tissue showed a diffuse hyperplasia of the Langerhans islet cells; indirect immunofluorescence in the presence of antigastrin antibodies was faintly positive and difficult to evaluate. However, gastrin levels clearly decrease after the operation may be because the inhibitory effect of total gastrectomy or because of the partial pancreatectomy. Furthermore, the inhibitory effect of tyrocalcitonine onthe pre- and postoperative gastrin levels measured by radioimmunoassay could be verified. For the moment the importance of this test in the diagnosis of Zollinger-Ellison syndrome, and especially in the diagnosis of ZES-type II, is not known.
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PMID:[Zollinger-Ellison syndrome type II due to diffuse hyperplasia of the pancreatic islet cells (author's transl)]. 38 7

Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
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PMID:Duodenal endocrine cells in adult coeliac disease. 38 55

The gastrointestinal contribution to carbohydrate metabolism includes carbohydrate absorption and the release of gastrointestinal hormones that interact with the endocrine pancreas. To learn the contributions to the enteroinsular axis from different levels of the gastrointestinal tract and different nutrients in chyme, we determined serum concentrations of glucose, gastric inhibitory peptide (GIP), insulin, and glucagon postprandially in six normal subjects who underwent diversion of chyme just proximal to an occlusive balloon at the ligament of Treitz and jejunal infusion of saline or chyme carbohydrate, protein, and lipid, separately or in combination. Postprandial elevations of serum glucose, GIP, and insulin and decrease of serum glucagon were elicited predominantly from the bowel and its contents distal to the ligament of Treitz. In this segment, each chyme nutrient (but especially carbohydrate) significantly stimulated factors affecting carbohydrate metabolism. Protein and lipid were able to block carbohydrate-induced glucagon inhibition. The gastroduodenal segment, although containing several proposed insulinotropic hormones (gastrin, secretin, and cholecystokinin), had no effect on serum glucose of glucagon and stimulated only small insulin and GIP responses.
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PMID:Intestinal nutrient influence on the enteroinsular axis. 40 Jul 36

Inhibiting effects of hypertonic glucose and amino-acids on pancreatic exocrine function were studied using mongrel dogs with chronic gastric and pancreatic fistulae. Under the basal stimulation with secretin and pancreoxymin, 20% glucose, 30% glucose and 12% amino acids were given intravenously. Infusion of these substances caused the maximal decreases in pancreatic juice volume and amylase output, to 23% and 11%, respectively (20% glucose), 32% and 29% (30% glucose), and 53% and 42% (12% amino acids). But no significant changes were noted in bicarbonate concentration. When glucose was infused, the rise in levels of blood sugar and IRI was associated with the inhibition of pancreatic exocrine secretion. Aminoacid infusion produced the greatest inhibitory effect on the pancreatic secretion and markedly elevated both the levels of IRI and IRG. Intravenous infusion of glucagon suppressed notably the exocrine function of the pancreas.
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PMID:Effects of hypertonic glucose and amino acid infusions on pancreatic exocrine function. 41 25


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