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)

1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin- and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat. 2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrin-stimulated secretion. CCK-PZ stimulated acid secretion at a low dose level but at higher doses it inhibited both pentagastrin- and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine- but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrin-stimulated acid secretion with little or no effect on the response to histamine. 3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -- findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.
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PMID:Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach. 610 65

The conformation of some polypeptides and proteins in sodium dodecyl sulfate (NaDodSO4) solutions was studied by circular dichroism. The type and extent of induced structure depend on their helix- and beta-forming potential. Anionic side groups in segments of helix or beta form tend to destabilize the ordered structure unless they are protonated. beta-Endorphin has one Glu inside a predicted helical segment; its helicity in a NaDodSO4 solution is enhanced at pH below 4. alpha-Melanocyte-stimulating hormone having a Glu in a beta segment undergoes a pH-induced coil to beta transition in 1.25 mM NaDodSO4 (excess surfactant will disrupt the beta form). Reduced somatostatin assumes a beta form in 2 mM NaDodSO4 and a partial helix in 25 mM NaDodSO4, both of which are unchanged in acidic pH because it lacks -COOH groups. The unordered gastrin with five consecutive Glu's becomes helical in a NaDodSO4 solution at pH 4. Neurotensin with one Glu has no structure-forming potential and is unordered in both neutral and acidic NaDodSO4 solutions. This charge effect also manifests in segments of ordered structure for polypeptides and proteins such as glucagon, cytochrome c, parvalbumin, ribonuclease A, and lysozyme. The effect is especially predominant in tropomyosin that is rich in clusters of anionic side groups. Its more than 90% helicity is reduced to about one-half in a neutral NaDodSO4 solution, but most of it can be restored by lowering the pH to 2.4.
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PMID:Ordered conformation of polypeptides and proteins in acidic dodecyl sulfate solution. 611 37

Using histological and immunhistochemical techniques, nine endocrine cell types were observed in the mucosa of the gastrointestinal tract of the toad, Bufo regularis, viz. enterochromaffin, somatostatin, glucagon, pancreatic polypeptide (PP), secretin, gastric inhibitory peptide (GIP), gastrin-C-terminal pentapeptide (GTPP), neurotensin and bombesin cells. The enterochromaffin cells were distributed throughout the gastrointestinal tract except the rectum. Somatostatin, glucagon, PP, secretin, GIP and GTPP cells were observed both in the stomach and in the small intestine. Neurotensin cells were seen only in the ileum and bombesin cells only in the pyloric and antral parts of the stomach. Immunostaining of consecutive sections did not reveal more than one polypeptide hormone in any of these cell types. It is concluded from the present results that the toad gastrointestinal mucosa contains endocrine cell types that are more or less homologous to those in the mammal alimentary tract, though some of them exhibit a different topographic distribution.
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PMID:Histological and immunohistochemical studies of the endocrine cells of the gastrointestinal mucosa of the toad (Bufo regularis). 611 16

The effects of neuropeptides on the release of immunoreactive somatostatin (SRIF) from the rat hypothalamus were examined in vitro using a perifusion system. Twelve hypothalamic halves of male rats were placed on a Sephadex G-25 column and continuously eluted with Krebs-Ringer bicarbonate buffer, poH 7.4, at 37 C. A high potassium concentration (56 mM) stimulated SRIF release in a calcium-dependent manner. The infusion of glucagon (10(-7), 5 x 10(-7), and 10(-6) M) resulted in a dose-related increase in the release of SRIF. Neurotensin (10(-6) M) also stimulated SRIF release, whereas vasoactive intestinal polypeptide (10(-7) and 10(-6) M) inhibited SRIF release. SRIF release was not affected by cholecystokinin-octapeptide (10(-6) M), cholecystokinin-tetrapeptide (10(-6) M), or tRH (10(-6) M). These findings suggest that SRIF release from the rat hypothalamus is influenced by glucagon, neurotensin, and vasoactive intestinal polypeptide.
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PMID:Effects of glucagon, Neurotensin, and vasoactive intestinal polypeptide on somatostatin release from perifused rat hypothalamus. 612 61

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.
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PMID:Neuropeptides and appetite: contribution of neuropharmacological modeling. 614 55

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

Neurotensin is a tridecapeptide originally isolated and characterized from bovine hypothalamus and later, in identical form, from bovine and human intestine. In the rat about 85% of immunoreactive neurotensin is found in the gut and about 10% in the brain. When an antibody specific for the amino terminal region of neurotensin was used the highest concentrations were found in the mucosa of the ileum, while an antibody specific for the biologically active region, the carboxyl terminus, also detected large amounts in the mucosa of the upper gastrointestinal tract. After a meal neurotensin - as measured by carboxyl terminal antibodies - rises after 5 min, a time in which the chymus has not yet reached the ileum, the main source of whole neurotensin. It is therefore possible that the carboxyl terminal molecules of neurotensin, found in the upper gastrointestinal tract, play an important physiological role. In plasma, neurotensin is rapidly degraded into smaller amino terminal and therefore biologically inactive molecules. Increases of carboxyl terminal neurotensin have been found in plasma in only a very few studies. The nature of this immunoreactive material has not yet been established. Therefore, the physiological role of neurotensin as a circulating hormone is unknown. Potential actions of neurotensin include thermoregulation, regulation of hormone release from brain (pituitary hormones) and gut (glucagon, insulin, somatostatin, pancreatic polypeptide), increase of vascular permeability, vasodilatation, inhibition of gastric acid secretion, stimulation of pancreatic secretion and changes of gut motility from the fasting to the fed type.
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PMID:[Neurotensin--what is known about its role as a hormone in the gastrointestinal tract?]. 647 77

In a pancreatic adenoma approximately 78.7% of the endocrine cells reacted specifically with antisera to neurotensin, 17.5% to gastrin, 2.8% to pancreatic polypeptide, and 1% to glucagon. The electron microscope revealed that the majority of the endocrine cells were N-cells--morphologically similar to the ileal N-cells which are known to represent the neurotensin-producing cells. Neurotensin was extracted from the tumor and identified by Sephadex, ion-exchange, and high-pressure liquid chromatography. Gastrin, pancreatic polypeptide, and glucagon cells were also identified by the electron microscope; the peptides were extracted and demonstrated by chromatography. The serum concentrations of these hormones were elevated. After total gastrectomy which was necessary because of Zollinger-Ellison syndrome, a jejunoesophageal alkaline reflux, reaching the upper esophagus appeared. As intravenous infusion of synthetic neurotensin in rats caused an increase of luminal enteric pressure, it is suggested that severe jejunoesophageal reflux after gastrectomy may be a clinical feature of a neurotensinoma.
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PMID:A multihormonal tumor of the pancreas producing neurotensin. 730 61

Neurotensin (NT), peptide YY (PYY), and several peptides derived from proglucagon are promptly released from endocrine cells of the distal part of the gut after oral ingestion of a meal, thus suggesting that release of these peptides is partly under neural and/or hormonal control. Our previous studies conducted with a model of isolated vascularly perfused rat colon showed that colonic L cells are highly responsive to several transmitters of the gut and to the hormonal peptide GIP. To test the possibility that hormones produced by the proximal small intestine or transmitters of the enteric nervous system may also modulate the secretory activity of the ileal L cells, various intestinal regulatory peptides and neurotransmitters were administered intraarterially for 30 min in the isolated vascularly perfused rat ileum preparation. The secretory activity of the ileal N cells was comparatively assessed. The release of NT, PYY, and glucagon-like peptide-1 (GLP-1) in the portal effluent was measured with specific RIAs. The muscarinic cholinergic agonist bethanechol at a concentration of 10(-4) M provoked a biphasic release of PYY, GLP-1, and NT, consisting of an early peak followed by a sustained response. Similarly, bombesin (10(-7) M) induced a marked biphasic release of PYY and GLP-1. In contrast, the NT response was essentially monophasic, characterized by an early peak secretion. Tetrodotoxin did not modify the bombesin-induced release of PYY, GLP-1, and NT. The beta-adrenergic agonist isoproterenol at a concentration of 10(-6) M induced a transient rise in portal PYY and GLP-1 concentrations, whereas the effect on NT release was clearly biphasic. Calcitonin gene-related peptide (5 x 10(-8) M) induced a dramatic rise in PYY, GLP-1, and NT immunoreactivities in the portal effluent (peaks at 600%, 500%, and 550% of the basal values, respectively, 4 mi n after the start of infusion). Intraarterial infusion of GIP over the concentration range (0.5-3 nM) evoked a significant increase in portal concentration of the three peptides only at the threshold concentration of 3 nM. Secretin (50 pM) or cholecystokinin (50 pM) did not affect the release of ileal hormones. In conclusion, ileal L and N cells respond to a variety of transmitters of the gut. The pattern of peptide release depends on the cell type studied. The two cosynthesized peptides, PYY and GLP-1, appear to be cosecreted in the conditions of the present study.
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PMID:Regulation of glucagon-like peptide-1-(7-36) amide, peptide YY, and neurotensin secretion by neurotransmitters and gut hormones in the isolated vascularly perfused rat ileum. 758 57

Fasting and postprandial plasma levels of the gut hormones gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide, motilin, neurotensin, peptide YY (PYY), enteroglucagon, glucagon, insulin, and pancreatic polypeptide were measured in 11 patients with alkaline gastritis associated with excessive duodenogastric reflux not related to previous gastric surgery (primary DGR), 12 primary DGR patients after pancreatico-biliary diversion ("duodenal switch" procedure), and in 10 age-matched healthy controls. Gastric emptying of a semisolid oatmeal was also measured in patients with primary DGR and in patients after bile diversion. Fasting plasma levels of the distal gut hormone neurotensin and the pancreatic islet hormone insulin were significantly greater in patients with primary DGR compared with controls. Neurotensin levels were normal in patients studied after bile diversion. Postprandial plasma levels, incremental integrated and total integrated responses for CCK, secretin, insulin, neurotensin, PYY, and enteroglucagon, were significantly greater in patients with primary DGR compared with controls. The majority of these responses normalized after bile diversion; however, the postprandial response for insulin and enteroglucagon remained elevated. Patients with primary DGR had a rapid early postprandial phase of gastric emptying of solids, which showed a significant correlation with plasma neurotensin levels. Bile diversion produced a significant delay in this lag-phase of gastric emptying. These abnormalities in gut regulatory hormones appear to be adaptive changes to rapid early postprandial gastric emptying, probably related to antropyloric dysmotility, which has been implicated in the pathogenesis of this condition. Measurement of these gastrointestinal hormones may become useful in the diagnosis of primary DGR.
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PMID:Abnormal plasma gut hormones in pathologic duodenogastric reflux and their response to surgery. 841 94


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