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)

The distribution and quantification of enteroendocrine cells exhibiting immunoreactivities to nine peptides and one amine were examined in the gastrointestinal mucosa of the adult opossum using specific immunocytochemical methods. In the stomach, 90% of the enteroendocrine cells are confined to the pyloric glands and this region contained 73% of the gastrin-containing cells, 60% of the somatostatin-containing cells and 9% of cells reactive for 5-HT. Enteroendocrine cells showing immunoreactivities to glucagon, pancreatic polypeptide, somatostatin and 5-HT were observed scattered within the oxyntic glands. Only somatostatin and 5-HT positive cells were found in the cardiac glands. Immunoreactivities to CCK, glucagon, gastrin, BPP, somatostatin, secretin, motilin, neurotensin, GIP and 5-HT were observed in the epithelium of the small intestine. Although considerable variation exists in the distribution of individual enteroendocrine cell types along the intestinal tract, nearly equal numbers of enteroendocrine cells were observed in each segment. The percentage of enteroendocrine cells increases distally in the colon. Of the three enteroendocrine cell types present, somatostatin- and 5-HT-immunoreactive cells are evenly distributed, whereas neurotensin-immunoreactive cells increase in numbers distally, resulting in an increase in total number.
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PMID:Quantitative distribution of enteroendocrine cells in the gastrointestinal tract of the adult opossum, Didelphis virginiana. 407 99

In the presence of 3-isobutyl-l-methylxanthine, VIP produced a dose-related (3 X 10(-9)-10(-7) M) increase (8-fold) in cAMP production in isolated HEp-2 cells incubated at 15 degrees C in KRP buffer. Among the peptides structurally related to VIP, including secretin (10(-7) M), pancreatic glucagon (10(-6) M), PHI, somatostatin-14 (10(-6) M), hpGRF (10(-8)-4 X 10(-6) M), GIP (2 X 10(-7) M), only PHI (3 X 10(-7) M and above) is able to activate the cAMP-generating system in HEp-2 cells, but at 10(2) times lower potency. Under the same conditions, histamine (10(-3) M) was also ineffective, while PGE2 (10(-7)-10(-4) M) increased (4-fold) basal cAMP levels in HEp-2 cells. The VIP effect is related to the interaction of the peptide on VIP recognition sites (125I-VIP-binding capacity), coupled to the membrane-bound adenylate cyclase. The results indicate that the transformed laryngeal cell line HEp-2 possesses a receptor-cAMP system preferentially activated by VIP (relative potencies: VIP greater than PHI much greater than other peptides of the secretin family), and suggest that this neuropeptide could modulate biological functions in normal laryngeal epithelia in man.
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PMID:Activation of the cAMP-generating system by vasoactive intestinal polypeptide (VIP) in the human laryngeal malignant cell line HEp-2. 608 15

The 24 endocrine pancreatic tumors and 14 carcinoids were examined immunohistochemically for cholecystokinin, insulin, gastrin, GIP, glucagon, sercretin, VIP, motilin, neurotensin, pancreatic polypeptide (PP), somatostatin, and ACTH. In 12 tumors of the pancreas more than one peptide-containing cell type was observed. The clinical symptoms showed hypersecretion of only one of the hormones, however. The midgut carcinoids (jejunum, appendix) represented the classical view of the carcinoid as an argentaffin cell tumor secreting 5-hydroxytryptamine. Tumors originating in the foregut (bronchus, stomach, duodenum) and hindgut carcinoids (rectum) were nonargentaffine, containing and secreting various polypeptide hormones. We conclude that light microscopic immunohistochemical methods are useful in distinguishing endocrine from nonendocrine tumors and multihormonal syndromes (MEA) in the classification of predominant hormone-secreting tumors.
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PMID:[Endocrine tumors of the gastrointestinal and pancreatic systems. Multiple endocrine adenoma from another viewpoint]. 610 39

In the Lausanne classification of islet cells which is based mainly on the ultrastructural characteristics of secretion granules, a total of nine different cell types have been described. By immunocytochemistry at least 12 different hormones or peptides have been either detected or postulated as being within cell types in the pancreatic islets. The cells responsible for the secretion of insulin, glucagon, GIP, pancreatic polypeptide and somatostatin have been firmly established. The identification of cells containing VIP, secretin, gastrin, biogenic amines and other peptides still remain tentative. The development of immunocytochemical techniques and their use at the light microscopic and ultrastructural level have been of immense value in the recognition of islet cell types and the peptides that they contain. Continued improvement in the purification of islet hormones and specific antibodies to these hormones together with correlative and immunocytochemical studies should lead to a better understanding of normal islet cell function, and thus hopefully, the cellular abnormalities encountered in tumors of the endocrine pancreas.
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PMID:Types of pancreatic islet cells and their immunocytochemical identification. 616 78

Using rabbit and guinea-pig antisera, raised against GEP neurohormonal peptides of mammalian origin, cells were observed in the brain and/or in the fused ventral ganglia of the last (fifth) larval instar of the hoverfly, Eristalis aeneus, being immunoreactive with antisera against insulin, somatostatin, glucagon, PP, secretin, gastrin/CCK/caerulein; substance P, enkephalin and endorphin. Most of these GEP neurohormonal peptides also occurred in nerve fibers. No immunoreactive cells or nerve fibers could be detected with antisera against GIP, VIP, (the central fragments of) CCK, bombesin or neurotensin. The antisera tested failed to reveal any immunoreactive cells or nerves in Weismann's ring (fused corpus allatum/corpus cardiacum and thoracic gland) or in different parts of the alimentary tract. The observations support the hypothesis that neuronal GEP hormonal peptide production in the brain is a genuinely original mechanism and the appearance of endocrine cells in the gut a later feature in evolution.
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PMID:Immunohistochemical evidence of gastro-entero-pancreatic neurohormonal peptides of vertebrate type in the nervous system of the larva of a dipteran insect, the hoverfly, Eristalis aeneus. 616 52

GIP (EC50 = 8 X 10(-9) M, 5-fold stimulation), pancreatic glucagon (EC50 = 10(-8)M, 13-fold) and porcine or chicken VIP (EC50 = 2.5 X 10(-9) M, 10-fold) are shown to activate the cAMP generating system in HGT -1 cells. Combinations of GIP, pancreatic glucagon and VIP indicate the occurrence of 3 separate sets of recognitions sites for these 3 peptides. Accordingly, chronic treatment of cultured HGT -1 cells by VIP (10(-8) M) during 6 days resulted in homologous desensitization of VIP receptor activity. Other peptides structurally related to the secretin-glucagon family, to neurotensin, or to gastrin are either ineffective or very weak agonist (hpGRF). GIP or pancreatic glucagon are inactive on the human colonic cell line HT-29, indicating the gastric specificity of the effect of GIP and glucagon in transformed epithelial cells originating from the human gastrointestinal tract. This implies that GIP and (pancreatic-entero) glucagon peptides may regulate gastric secretions directly, under similar mechanisms that those we evidenced in the rat.
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PMID:Gastric inhibitory peptide (GIP), pancreatic glucagon and vasoactive intestinal peptide (VIP) are cAMP-inducing hormones in the human gastric cancer cell line HGT-1. Homologous desensitization of VIP receptor activity. 632 77

125I-GIP binds reversibly to a high affinity binding site in crude plasma membranes prepared from a hamster pancreatic beta cell tumor. The treatment of labeled membranes with the cross-linker dithiobis (succinimidylpropionate) prevents, to a greater extent, the rapid dissociation of 125I-GIP-membrane complexes which is observed when 10(-6) M native GIP is added. Polyacrylamide gel electrophoresis of membrane proteins reveals a major 125I-GIP-protein complex of Mr 64,000. This labeling decreases when increasing concentrations (10(-9) -10(-6)M) of native GIP are added but is not altered by other peptide hormones (tested at 10(-6)M) including glucagon, VIP and insulin. The Mr 64,000 complex is not observed in tissues which have no specific binding sites for GIP such as intestinal epithelium. Assuming one molecule of 125I-GIP is bound per molecule of protein, one protein with Mr 59,000 is identified as the specific GIP binding site.
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PMID:The GIP receptor on pancreatic beta cell tumor: molecular identification by covalent cross-linking. 633 48

To study the role of enteroinsular hormones in fetal macrosomia and neonatal hypoglycemia in infants of diabetic mothers, we measured plasma concentrations of free and total immunoreactive insulin, C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide at birth in 35 IDMs and 35 infants of normal mothers. Twenty fasting adults of normal weight were also studied. Sixteen IDMs were macrosomic at birth; 17 developed neonatal hypoglycemia over the first postnatal hours. The IDMs had ten times higher concentrations of free IRI than the normal infants in cord blood. Free IRI concentrations were related to the severity of maternal diabetes, with the infants of white class D to F mothers having the highest levels. The IDMs with macrosomia had a twofold increase in the concentrations of free IRI when compared with IDMs of normal weight. There was a significant correlation between the birth weight ratio and the concentrations of free IRI. The IDMs who developed neonatal hypoglycemia had considerably higher concentrations of free IRI than did normoglycemic IDMs. The decrease of blood glucose over the first postnatal hours correlated strongly with the free IRI concentrations in the cord blood. The IDMs had a threefold increase of the C-peptide concentrations over those in normal infants. Six IDMs had a molar ratio of C-peptide to free IRI of less than 1. Both the IDMs and normal infants had substantially higher concentrations of enteroglucagon and lower concentrations of GIP than did the fasting adults. Our data provide direct evidence that IDMs are markedly hyperinsulinemic at birth and that ambient hyperinsulinemia plays a crucial role in the development of fetal macrosomia and neonatal hypoglycemia. Moreover, the observed discrepancy in the relative increase of free IRI and C-peptide, combined with the low molar ratio of C-peptide to IRI, suggests a decreased metabolic clearance of insulin or transplacental passage of insulin from the maternal circulation in infants of mothers with insulin-treated diabetes.
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PMID:Relation of enteroinsular hormones at birth to macrosomia and neonatal hypoglycemia in infants of diabetic mothers. 635 86

L-tryptophan was given to fasted rats intragastrically or intravenously at a dose of 500 of 166 mg/kg b.w., respectively. Mean (+/- SEM) plasma insulin levels rose after both stimuli and at 10, 30 and 45 min were 63 +/- 26, 86 +/- 25, 48 +/- 7 mU/l after oral, and 28 +/- 4, 25 +/- 6, 19 +/- 6 mU/l after intravenous administration, respectively; plasma tryptophan levels at the above intervals during the oral study were 27%, 60% and 128%, respectively of those during the intravenous study. Plasma GIP levels rose only after intragastric tryptophan administration, and plasma GLI levels did not change in response to either intragastric or intravenous tryptophan. Intragastric tryptophan consistently raised plasma pancreatic glucagon levels which were significantly higher than those observed in control rats given saline, 5, 10, 30 and 45 min after administration. The rise in plasma glucagon was attributed to the glucagonotropic effect of GIP.
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PMID:The differential effect of intragastric and intravenous tryptophan on plasma glucose, insulin, glucagon, GLI and GIP in the fasted rat. 637 8

The surface epithelial cells of the stomach and duodenum secrete bicarbonate at rest and in response to a number of agonists including the gastrointestinal hormones, glucagon, and GIP. Since those hormones with structural homology may have similar effects, the purpose of the present study was to examine the effect of graded doses (6, 24, and 96 nmol/kg) of pure porcine secretin, VIP, and PHI on bicarbonate secretion by the proximal duodenum containing Brunner's glands. Experiments were performed in vivo on unanesthetized Sprague-Dawley rats with chronic Thiry-Vella type loops of the proximal 2 cm of duodenum. The order of testing was random and only one hormone was tested on a single day. Compared to the saline control, each dose of VIP produced a significant increase in duodenal bicarbonate secretion in a dose-response manner. The two higher doses of secretin and only the 96 nmol/kg dose of PHI significantly increased bicarbonate output. The responses to 96 nmol/kg dose of secretin and VIP were similar, and each was significantly greater than observed with PHI. It is concluded that secretin and VIP stimulate proximal duodenal bicarbonate secretion and are more potent than PHI.
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PMID:Secretin, VIP, and PHI stimulate rat proximal duodenal surface epithelial bicarbonate secretion in vivo. 654 70


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