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 synergistic impact of glucagon-like peptide-1 (GLP-1) (7-36)amide and cholecystokinin-8 (CCK-8) was studied in the rat pancreas. The GLP-1 (7-36)amide (1 pM-1 microM) had no effect on the basal or CCK-stimulated (1 nM-1 pM) amylase release from isolated pancreatic acini. The insulinotropic action of 0.5 nM GLP-1 (7-36)amide, which weakly stimulated the glucose-induced (6.7 mM) insulin release from the isolated perfused rat pancreas, was strongly potentiated by the addition of CCK-8 (20, 50, and 100 pM) to the perfusate. In concentrations as they occur physiologically after a meal, CCK-8 alone had no significant effect on basal or glucose-stimulated (6.7 mM) insulin secretion. Our data support the assumption that the nutrient-regulated intestinal release of various peptides represents a regulatory system to ensure an adequate insulin response to food intake, at least in rats.
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PMID:Interaction of glucagon-like peptide-1 (7-36)amide and cholecystokinin-8 in the endocrine and exocrine rat pancreas. 169 1

Galanin, a 29 amino acid neuropeptide, was recently isolated from pig intestine. We studied the localization, nature and effect of galanin in pig pancreas. Galanin immunoreactive nerve fibers were regularly found in the pancreas. A peptide chromatographically similar to synthetic galanin was identified in pancreas extracts. The effect of galanin on the endocrine and exocrine secretion was studied in isolated pancreases, perfused with a synthetic medium containing 3.5, 5 or 8 mmol/l glucose and synthetic galanin (10(-10)-10(-8) mol/l). There was no effect on the basal exocrine secretion. The output of insulin, glucagon, somatostatin and pancreatic polypeptide (PP) was measured in the effluent. There was no effect on PP secretion. At a perfusate glucose concentration of 5 mmol/l, galanin at 10(-9) mol/l increased insulin secretion by 55 +/- 14% (mean +/- S.E.M., n = 5) of basal secretion, and at 10(-8) mol/l by 58 +/- 27% (n = 6). At 8 mmol/l glucose, insulin secretion increased by 25 +/- 10% (n = 6) and 62 +/- 17% (n = 8). At 5 mmol/l glucose glucagon secretion was increased by 15 +/- 3% (n = 5) by galanin at 10(-9) mol/l and by 29 +/- 11% (n = 5) by galanin at 10(-8) mol/l, and at 8 mmol/l glucose by 66 +/- 27% and 41 +/- 25%. Somatostatin secretion was inhibited to 72 +/- 2% (n = 5) of basal secretion by galanin at 10(-9) mol/l and to 65 +/- 7% (n = 7) at galanin at 10(-8) mol/l, both at 5 mmol/l glucose. At 8 mmol/l the figures were 83 +/- 6% and 70 +/- 10%. Insulin secretion in response to square wave increases in glucose concentration from 3.5 to 11 mmol/l (n = 5) increased 2-fold during simultaneous perfusion with galanin (10(-8) mol/l).
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PMID:Galanin in the porcine pancreas. 169 4

The influence of essential fatty acid (EFA) deficiency on pancreatic endocrine and exocrine function was studied in 120-day-old rats. The plasma insulin response was determined after in vivo administration of glucose and arginine. The plasma glucagon response was assessed after infusion of arginine. Islet peptides were examined by immunocytochemistry. The exocrine function of pancreas was studied by amylase secretion in isolated pancreatic acinar cells after stimulation with the cholinergic agonist carbacholine chloride. The EFA-deficient (EFAD) rats showed higher basal plasma insulin concentrations and lower basal glucose levels than control rats (P less than .01 and P less than .01, respectively). The plasma insulin response to glucose was potentiated in the EFAD rats (P less than .001). Both insulin and glucagon responses to arginine were normal. The isolated pancreatic acinar cells showed a low basal amylase secretion, but a normal response to carbacholine chloride. There were no overt morphological changes seen in the pancreas and the immunocytochemical staining pattern of insulin, glucagon, somatostatin, and pancreatic polypeptide cells did not differ from controls. The results of the study show that the secretory function of the endocrine and exocrine pancreas is operational in EFA deficiency. The EFA deficiency was accompanied by a basal hyperinsulinemia and hypoglycemia and an exaggerated insulin response to glucose, the pathophysiology of which has to be further studied.
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PMID:Pancreatic function in the essential fatty acid deficient rat. 169 88

A spontaneously developed endocrine-exocrine pancreatic dysfunction was observed in the aged males of an inbred strain of Wistar rats, WBN/Kob. Nonobese male WBN/Kob rats developed glycosuria and hyperglycemia at around 9 months of age. Cumulative incidence of diabetes in male rats was 43% (33 of 76) at 12 months of age and reached 90% at the age of 21 months. In contrast, female rats did not become diabetic. Urinary excretion of amylase in WBN/Kob rats was significantly increased in comparison with control Wistar rats. Moreover, the exocrine pancreatic function test was impaired in WBN/Kob rats. Pathological examination of pancreata revealed infiltration of inflammatory cells, hemorrhage, deposition of hemosiderin, and fibrinous exudation around pancreatic ducts and blood vessels at 3 months of age. A gradual increase of fibrous tissue into the exocrine tissue and islets was observed with advancing age. The extremely enlarged interlobular lymph nodes were also observed. At the age of 12 months, the fibrous tissue replaced extensive areas of the pancreas and involved islets. The amylase content of pancreata in WBN/Kob rats was markedly decreased in comparison with that in Wistar rats at 12 months of age. Islets composed of few endocrine cells were detected. Immunohistochemical staining for insulin and glucagon showed a decreased number of not only B cells but also A cells. Moreover, both the pancreatic insulin and glucagon contents were markedly decreased in WBN/Kob rats in comparison with Wistar rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic strain (WBN/Kob) of rat characterized by endocrine-exocrine pancreatic impairment due to distinct fibrosis. 169 84

An amino-terminal histidyl structure (His1) is characteristic of most peptides in the glucagon superfamily. An assay for His1 peptides performed by amino-terminal amino acid sequencing was used to screen venom from the Gila monster lizard, Heloderma horridum. Two His1 peptides were identified: helospectin and a new His1 peptide that has been named exendin-3 to indicate that it is the third peptide to be found in an exocrine secretion of Heloderma lizards which has endocrine activity, the first two being helospectin (exendin-1) and helodermin (exendin-2). In the lot of H. horridum venom tested, exendin-3 was 5-10-fold more abundant in molar concentration than helospectin. The structure of exendin-3 was analyzed by amino acid sequencing and mass spectrometry. Exendin-3 is a 39-amino acid peptide with a mass of 4200. It contains a carboxyl-terminal amide and has a strong homology with secretin at its amino-terminal 12 amino acids. The complete structure of exendin-3 is His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Asp-Leu-Ser-Lys-Gln-Met-Glu-Glu-Glu-Ala- Val-Arg - Leu-Phe-Ile-Glu-Trp-Leu-Lys-Asn-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro- Ser- amide. It is 32 and 26% homologous with helospectin and helodermin, respectively. It has greatest homology with glucagon (48%) and human glucagon-like peptide-1 (50%). Exendin-3 (3 microM) stimulated increases in cellular cAMP and amylase release from dispersed guinea pig pancreatic acini.
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PMID:Purification and structure of exendin-3, a new pancreatic secretagogue isolated from Heloderma horridum venom. 170 Jul 85

Availability of specific cholecystokinin (CCK) receptor antagonists has the potential for contributing to delineation of the role of CCK in the development of pancreatitis and, perhaps, development of new therapeutic agents for treatment of the disorder. The purpose of this study was to evaluate the effect of a potent CCK receptor antagonist, CR 1409, on bile reflux pancreatitis. The opossum pancreatic duct enters the common duct in such a position that it is possible to ligate the common duct distal to the pancreatic duct, resulting in bile refluxing into the pancreatic duct and producing pancreatitis. CR 1409 was administered to opossums at the time of distal common duct ligation and at the time of cystic- and common ducts ligations. In a separate group, CR 1409 administration was begun 24 hours following onset of pancreatitis. Control experiments were performed, in which CR-1409 was not administered. Serum amylase, pancreas gland weights, inflammation, and systemic venous insulin, glucagon, and CCK concentrations were evaluated. Bile duct ligation resulted in significant hyperamylasemia, pancreas gland edema, inflammation, hyperglucagonemia, hypercholecystokinemia, and hypoinsulinemia. CR 1409, administered at the onset of pancreatitis, significantly decreased amylase concentrations, gland weight, and inflammation, when compared to control values. Hormonal changes associated with pancreatitis were also significantly altered by CR 1409 administration. When administered 24 hours following onset of pancreatitis, CR 1409 was not effective in altering the pancreatitis produced by bile duct ligation. The results suggest that CCK plays a permissive or contributory role in the inflammatory process and in associated hormonal changes during development of bile reflux pancreatitis in the opossum.
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PMID:The effect of the CCK receptor antagonist CR 1409 on bile reflux pancreatitis in the opossum. 171 73

Forty resected cases of heterotopic pancreas (15 of Heinrich's type I and 25 of type II) in the stomach were investigated. Acinic cells were more remarkably positive by pancreatic polypeptide and amylase in the cases of type I consisting of acinic cells, ducts and islet cells compared with those in type II consisting of acinic cells and ducts. Staining behavior by insulin, gastrin, glucagon, somatostatin and serotonin was similar to that of normal pancreas. However, the intestinal epithelium containing goblet cells and pyloric gland-like glands consisting of the cells with clear cytoplasm were not infrequently produced from the ducts in the lesions of type II. Muscle fibers with transition to muscularis mucosae were more frequently intermingled in the lesions of type II compared with type I. Acinic cell-differentiation in the mucosa apart from the main lesion was found in several cases of type II. It was suspected that there are two types of histogenesis for the heterotopic pancreas in the stomach; one arises from the fetal immigration of pancreas tissue in the stomach and the other from the immature gastric mucosal penetration into the submucosa with secondary differentiation to the pancreas tissue.
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PMID:[Histological study of heterotopic pancreas tissue of the stomach--histogenesis and immunohistochemical findings]. 192 Aug 87

Retrograded amylose was prepared by gelatinization of high amylose cornstarch, followed by storage at 1 degrees C for 48 h. The insoluble residue, which resisted hydrolysis with porcine amylase, was dried and fed to male Wistar rats for 14 d in powdered semisynthetic diet. Control rats received a similar diet containing sucrose in place of resistant starch. Fecal collections were performed throughout the feeding period. After 14 d the animals were killed. The small intestine and cecum were removed for morphological examination, measurement of small intestinal crypt cell production rate (CCPR) and analysis of luminal carbohydrate content. Blood samples were collected for analysis of cholesterol, glucagon, and enteroglucagon. In the starch-fed rats, fecal bulk and excretion of starch were higher than in the controls, but they declined markedly over the feeding period. Cecal size and contents were also greater in the starch-fed rats, and cecal pH was significantly lower. The CCPR was 66% higher in the ileum of the starch-fed rats (P less than 0.001), but there was no difference in the jejunum. There were no differences in serum cholesterol or enteroglucagon levels. We conclude that retrograded amylose is partially degraded in the alimentary tract of rats, but it contributes significantly to fecal bulk.
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PMID:Physiological effects of retrograded, alpha-amylase-resistant cornstarch in rats. 199 56

In an effort to establish diagnostic criteria for rejection and recurrent disease in transplanted pancreas, a comparative study was performed based on clinical diagnosis. Clinical rejection was diagnosed in patients who had decreased urinary amylase or increased blood glucose; they were treated for rejection and improved. A clinical diagnosis of recurrent diabetes was made in syngeneic transplant recipients with islet dysfunction. In addition, two control groups were used--nontransplant, nondiabetic pancreatitis patients and pretransplant normal biopsies from patients in the study. Morphologically, tissues were assessed for acinar inflammation, ductal changes, islet and nerve inflammation, and vascular changes. Immunohistochemical staining for insulin and glucagon was also performed to quantitate differences between the groups. Vascular changes (endothelialitis, vasculitis, obliterative endarteritis) were specific for rejection. Also, rejection was characterized by a lymphocytic or mixed infiltrate that involved the ducts. Recurrent diabetes was characterized by selective loss of beta cells with isletitis. Leukocyte common antigen and UCHL1 staining was helpful in identifying islet inflammation. An insulin/glucagon ratio of less than 1.0 appears to be specific for recurrent disease and in the absence of isletitis is a reasonable method for detecting recurrent disease at an early stage.
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PMID:Pancreas transplant pathology. A morphologic, immunohistochemical, and electron microscopic comparison of allogeneic grafts with rejection, syngeneic grafts, and chronic pancreatitis. 199 30

An immunohistochemical study for islet amyloid polypeptide (IAPP) was made on the gastrointestinal (GI) tract and pancreas of man and rat, using antisera raised against a synthetic peptide of C-terminal human IAPP (24-37) and a synthetic peptide of rat IAPP (18-37). A large number of IAPP-immunoreactive cells were found in the pyloric antrum, and a small number in the body of the stomach in both man and rat. Cytoplasmic processes extended out from the bipolar peripheral region of the immunoreactive cells, rather like neuronal processes, and some appeared to make contact with other immunoreactive cells. In addition, small numbers of immunoreactive cells were also seen in the duodenum and rectum, whereas they were absent from the jejunum, ileum and large intestine. An examination was made for evidence of colocalization of IAPP-immunoreactive material with material immunoreactive for gastrin, somatostatin, vasoactive intestinal polypeptide, pancreatic polypeptide, insulin, and glucagon, but none was found. IAPP-immunoreactive cells were also found in the pancreas of non-diabetic and non-insulin-dependent diabetic patients, but they were completely absent from a patient with insulin-dependent diabetes mellitus despite the presence of IAPP in the plasma. The results of these studies suggest that the peptide may have a biological role in situ in the GI tract and, in addition to the pancreas, may be a possible source of plasma IAPP.
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PMID:Islet amyloid polypeptide (IAPP) in the gastrointestinal tract and pancreas of man and rat. 207 50


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