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)

Fasting gastrointestinal motor and hormone patterns were studied in 11 healthy volunteers. Cyclic motor activity was present in all subjects during fasting, but the duration and site of onset of each cycle were variable, even in the same subject. Fasting gastrin, GIP, and glucagon levels remained low and constant during the 8-hr study, while plasma motilin levels exhibited cyclic variation in 7 of the 11 subjects. Achlorhydria (induced with cimetidine in 5 of the 11 subjects) did not alter the pattern of fasting motor activity or plasma motilin. In the remaining six subjects, the effect of liquid nutrient meals was examined. Ingestion of a sodium chloride bolus failed to disrupt fasting cyclic activity, while all nutrient-containing solutions inhibited gastric phase-2 motor activity, the duration of inhibition being longest for the mixed and lipid meals. All nutrient meals released GIP, while only protein and mixed meals released gastrin, and the lipid meal released motilin. Our study confirms the rhythmicity of interdigestive motor cycles in man and demonstrates their lack of dependence on gastric acid secretion and some relationship to motilin cycles in certain individuals as determined by radioimmunoassay. Transition from fasting to fed pattern (after liquid meals) is characterized by the inhibition of phasic gastric pressure changes in the antrum and the development of irregular activity in the intestine, similar in pattern to fasting phase 2. Because the duration of interruption of the gastric interdigestive pattern by meals depends on their nutrient content, we conclude that dietary composition may be a major determinant of the fasting-fed motor balance in man.
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PMID:Human interdigestive and postprandial gastrointestinal motor and gastrointestinal hormone patterns. 706 84

Secretin-like cells have been detected in the digestive tract of the ascidian Styela plicata by means of immunofluorescent and immunocytochemical methods. Especially, in the esophageal epithelium there are immunoreactive cells (S2) in which a biogenic amine (5-HT) and a regulatory peptide (secretin) occur together. In the gastric epithelium only secretin-like cells (S1) are present. Tests of cross-reactivity performed with glucagon, GIP and VIP, have confirmed the presence of a secretin-like molecule only in the S1 and S2 cells.
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PMID:Occurrence of different secretin-like cells in the digestive tract of the ascidian Styela plicata (Urochordata, Ascidiacea). 712 22

A specific and sensitive radioimmunoassay of human vasoactive intestinal polypeptide using synthetic VIP as standard preparation and antiserum to synthetic VIP R 502 (Yanaihara et al. 15) is described. No crossreactions with a number of other gastrointestinal hormones such as glucagon, secretin, GIP, HPP or substance P was detected. Aprotinin (Trasylol, Bayer) or heparin had no influence on the antigen--antibody reaction. High concentrations of sodium or potassium chloride in plasma, or hyperlipoproteinemia, did not interfere with the antiserum in the described system. Basal plasma concentration of VIP in 18 females (means +/- sem = 24.05 +/- 1.79 VIP/l) and 20 males (means +/- sem = 24.11 +/- 1.91 pmol/l VIP) showed no sex specific variations. During gastroscopy plasma VIP levels were significantly higher than basal values, showing a peak secretion when the gastric antrum was inspected. During the entire colonoscopic examination, VIP levels were significantly higher than basal values. Endoscopic examination may possibly liberate VIP from the VIP containing cells which can be found throughout the gastrointestinal tract.
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PMID:Radioimmunoassay for vasoactive intestinal polypeptide (VIP) in plasma before and during endoscopic examinations. 712 38

Membrane adenylate cyclase from rat heart was activated by the two gut peptides secretin and vasoactive intestinal peptide (VIP), glucagon, and the beta-adrenergic drug isoproterenol, in the presence of guanosine 5'-triphosphate (GTP). With all the stimuli tested, the optimal magnesium concentration was 5 mM, i.e. in excess over the 0.5 mM ATP substrate concentration and 0.01 mM GTP used as cofactor. Under these conditions, half-maximal adenylate cyclase activation with glucagon, secretin, and VIP was achieved at concentrations of 0.5, 0.5 and 1.0 microM, respectively. Data obtained with the secretin (7--27) fragment, a secretin antagonist, indicate that secretin and VIP acted on the same binding sites, which differed from glucagon binding sites. Structural requirements for secretin activation of cardiac adenylate cyclase were evaluated by comparing the potency and efficacy of parent peptides and synthetic analogs. The gastric inhibitory peptide GIP was inactive. When using 13 mono-or bi-substituted analogs, it appeared that amino acids in positions 1, 2, 3, 4 and 6 were of major importance while those in position 5 and 11 played a relatively minor role.
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PMID:Secretin and VIP-stimulated adenylate cyclase from rat heart. I. General properties and structural requirements for enzyme activation. 719 63

In eight totally pancreatectomised patients the release of the relevant gut hormones was determined after a standard test meal. Plasma levels of pancreatic glucagon were not significantly different from zero in our series of pancreatectomised patients. Pancreatic polypeptide was undetectable. These findings imply the absence of a significant number of normally functioning alpha cells and pancreatic polypeptide cells in extrapancreatic sites in man. Consistent with the antrectomy, duodenectomy, and resection of the upper jejunum that are performed in conjunction with a total pancreatectomy the gastrin release was significantly impaired. In contrast there was a striking post-prandial rise in enteroglucagon probably induced by the rapid intestinal transit time often seen after partial gastrectomy. In contrast plasma motilin and GIP levels were normal. Pancreatectomised man thus presents an interesting model of total deficiency of endogenous insulin, pancreatic polypeptide, and pancreatic glucagon and, in addition, greatly diminished gastrin. The considerable derangement of metabolic and intestinal function that follows total pancreatectomy may, in part, be explained by this gross disturbance of the normal physiology of gut hormone.
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PMID:Gut-hormone profile in totally pancreatectomised patients. 721 41

In 11 conscious volunteers, the jejunal absorption was measured during basal state and during the simultaneous intravenous infusion of small doses of gastrin, secretin, cholecystokinin, glucagon and gastric inhibitory polypeptide. The blood levels of gastrin, secretin, glucagon, and GIP were measured by RIA and were close to those achieved after a meal. The basal net absorption of water and electrolytes was reversed to a net secretion during the hormonal infusion. These results suggest that the jejunal secretion observed after a meal in man may be mediated by hormones released by the meal.
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PMID:Effect of a combination of gastrin, secretin, cholecystokinin, glucagon, and gastric inhibitory polypeptide on jejunal absorption in man. 742 91

Amylin inhibits glucose-induced insulin secretion in the rat pancreas. To study the mechanism by which amylin acts on the B-cell, we have investigated, in the perfused rat pancreas, the effect of synthetic rat amylin (75 pM) on insulin release elicited by secretagogues acting on the B-cell via the adenylate cyclase/cAMP system, i.e., glucagon (10 nM), gastric inhibitory polypeptide (GIP, 1 nM), forskolin (1 microM) and isobutylmethylxanthine (IBMX, 75 microM). In addition, we examined the effect of amylin on GIP-induced insulin release in pancreata from rats pretreated with pertussis toxin, an agent which inactivates certain Gi proteins coupled to adenylate cyclase. Amylin inhibited the insulin response to glucagon (approx. 70%), GIP (approx. 90%), IBMX (approx. 75%) as well as the early phase of forskolin-induced insulin output (approx. 74%). However, amylin failed to modify GIP-induced insulin release in pancreata obtained from pertussis toxin pretreated rats. These results would indicate that the inhibitory effect of amylin on insulin secretion could be, at least in part, attributed to its interfering with the adenylate cyclase/cAMP system. Furthermore, prevention of the inhibitory effect of amylin on GIP-induced insulin output by pertussis toxin pretreatment, supports the concept that amylin can inhibit insulin release via a pertussis toxin-sensitive Gi protein coupled to the adenylate cyclase system.
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PMID:Amylin (islet amyloid polypeptide) inhibition of insulin release in the perfused rat pancreas: implication of the adenylate cyclase/cAMP system. 751 1

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

A receptor capable of recognizing VIP-related peptides with unusual functional characteristics and selectivity profile was characterized on human IGR37 melanoma cells. When using either [125I]VIP or [125I]N-AcPACAP27 as a tracer, PACAP38 had the highest affinity, while PACAP27, VIP, helodermin, GRF and the VIP fragment VIP10-28 showed the same low affinity. Moreover, this receptor did not recognize PHM, PHV, helospectin, secretin, GIP, glucagon and glucagon-like peptide-1(7-36). Surprisingly, none of the peptides significantly stimulated the cAMP production. By covalent crosslinking, the receptor was shown to have a M(r) = 60,500.
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PMID:A receptor for VIP-related peptides with an unusual selectivity profile on the melanoma cell line IGR37. 770 17

Basic research on the cellular mechanisms that control the expression of the gene encoding glucagon has led to the discovery of proglucagon, which is processed alternatively by tissue-specific proteolysis to produce glucagon in the pancreatic alpha cells and a GLP-1 in the intestines. GLP-1 hormone is released into the circulation from intestinal L cells in response to meals and is the most potent incretin hormone known; GLP-1 and GIP appear to account for most, if not all, of the intestinal incretin effect in the augmentation of glucose-stimulated insulin secretion. Analyses of the mechanisms of action of GLP-1 and of glucose on isolated cultured rat beta cells using patch-clamp techniques to record ion channel activities has led to the glucose competence concept in which the combined glucose-signaling and GLP-1/cAMP-signaling pathways are required to affect depolarization of beta cells and to thereby stimulate insulin secretion. It is hypothesized that, among other possible target channels, the K-ATP channel is key first event in GLP-1/glucose-mediated activation of the beta cell secretory response. It is proposed that at least one factor contributing to the pathogenesis of NIDDM is a desensitization of the GLP-1 receptor on beta cells induced by the hypersecretion of GLP-1. Because of the discoveries that GLP-1 stimulates both secretion and production of insulin, and that the actions of GLP-1 are entirely glucose-dependent, GLP-1 may provide unique advantages over the sulfonylurea drugs in the treatment of NIDDM.
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PMID:The incretin notion and its relevance to diabetes. 812 72


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