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 effect of injection of glycogenolytic enzymes on tissue glycogen, blood glucose and plasma insulin was studied in mice. No effects were observed following phosphorylase, whereas the hydrolytic enzymes, alpha-amylase and acid amyloglucosidase depressed liver glycogen. In addition acid amyloglucosidase induced a decrease in blood glucose, a slight elevation of plasma insulin and a marked increase in tolbutamide-stimulated insulin release. At the doses given none of the enzymes affected muscle glycogen. Amyloglucosidase pretreatment markedly enhanced insulin release induced by glibenclamide, leucine, isoleucine, lysine and glucose whereas insulin release stimulated by IPNA, ACTH, glucagon and "CCK-PZ" was unaffected. Injection of acid amyloglucosidase has a profound influence on carbohydrate content and regulation in mice. It is suggested that the dependence or independence of amyloglucosidase activity among the insulin secretagogues tested might reflect different or partially different mechanisms in the process of insulin secretion.
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PMID:Carbohydrate content and regulation following injection of different glycogenolytic enzymes. 16 77

Because of the unique features of the ruminant digestive system, variations in diet composition and intake produce dramatic changes in ruminal fermentation. Optimizing nutritional management requires an understanding of how these variations and changes influence digestion and metabolism. Although the pancreas plays a central role in digestion and subsequent nutrient metabolism, relatively little is known about pancreatic adaptation to nutritional changes in the ruminant. Increasing starch intake has been suggested to increase pancreatic alpha-amylase; however, recent work suggests that dietary energy per se may drive these changes, and interactions with other nutrients, such as protein, may exist. Studies describing the influence of altered protein and lipid intakes on pancreatic adaptation in ruminants are lacking. Pancreatic secretion of both insulin and glucagon respond to the intravenous infusion of VFA in a dramatic fashion; however, feeding studies suggest that the influence of VFA on insulin and glucagon may be more subtle. Interactions exist between stimulatory signals and physiological state, such as lactation. Assessment of pancreatic endocrine secretion is further complicated by a variable removal of insulin and glucagon by hepatic tissues. These studies point out that pancreatic hormone secretion is controlled by integrated and complex mechanisms. Studies of these controlling mechanisms should consider the entire array to more fully understand hormone secretion.
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PMID:Impact of nutrition on pancreatic exocrine and endocrine secretion in ruminants: a review. 158 58

One thousand consecutively autopsied livers were examined for intrahepatic heterotopic pancreas. Heterotopic pancreas in the liver was found in 41 (4.1%) of the 1000 livers. It occurred with nearly equal frequency in "normal" livers and variously diseased livers. Histologically, heterotopic pancreas was situated exclusively in the large- and medium-sized portal tracts, and its size ranged from 250-900 microns in diameter. It was intermingled with intrahepatic peribiliary glands and appeared to communicate with bile duct lumina. Heterotopic pancreas consisted of three cell types: acinar cells with eosinophilic zymogenlike granules, clear cells resembling centriacinar cells, and ductular elements. Langerhans' islets were not found in any cases. Immunohistochemically, constituent cells of heterotopic pancreas contained pancreatic alpha-amylase and trypsin but lacked argentaffin and argyrophilic cells as well as insulin-, glucagon-, and somatostatin-immunoreactive endocrine cells. Ultrastructurally, acinar cells contained many dense granules regarded as zymogen granules. It is indicated that intrahepatic heterotopic pancreas occurs in large portal tracts. It may modify hepatic bile by secreting pancreatic enzymes into intrahepatic bile duct lumina.
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PMID:Pathologic observations of intrahepatic peribiliary glands in 1000 consecutive autopsy livers. Heterotopic pancreas in the liver. 218 71

Rye flakes, rye bread and white wheat bread were given as suspensions to rats and in standardized breakfast meals to non-insulin-dependent diabetics. In both cases the postprandial glucose response was lower after rye bread than after wheat bread. A larger amount of starch remained in the stomach of the rats 15 min after ingesting rye bread compared to wheat bread, indicating that delayed gastric emptying may be one factor explaining the lower response after rye bread. Although the incremental postprandial glucose areas after rye flakes and wheat bread were similar, the rate of decrease of the glucose curve was slower after flaked rye. This would point to a prolonged absorption of some starch in the rye flakes, also indicated by higher late immunoreactive insulin (IRI) values after that product. In the rats the content of starch in the stomachs 15 min after feeding was higher after rye flakes compared to wheat bread. In vitro incubations with alpha-amylase showed lower availability of the starch in rye flakes than in the breads, indicating that several factors may contribute to the differential postprandial glucose response after the wheat and rye products. The levels of insulin, C-peptide, gastric inhibitory polypeptide (GIP), glucagon, somatostatin, triglyceride and glycerol were followed after the breakfast meals. No pronounced differences of these parameters were seen. However, wheat bread gave significantly higher glucagon and GIP responses than did rye flakes. In conclusion, the absorption pattern and metabolic response after rye bread seems preferable to that after wheat bread. The flaked rye on the other hand was not effective in reducing postprandial glycaemia despite a lower availability of starch in vitro.
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PMID:Rye products in the diabetic diet. Postprandial glucose and hormonal responses in non-insulin-dependent diabetic patients as compared to starch availability in vitro and experiments in rats. 243 70

Mechanisms of glycogenolysis have been investigated in a comparative study with Wistar rats and gsd rats, which maintain a high glycogen concentration in the liver as a result of a genetic deficiency of phosphorylase kinase. In Wistar hepatocytes the rate of glycogenolysis, as modulated by glucagon and by glucose, was proportional to the concentration of phosphorylase a. In suspensions of gsd hepatocytes the rate of glycogenolysis was far too high as compared with the low level of phosphorylase a; in addition, only a minor fraction of the glycogen lost was recovered as glucose and lactate, owing to the accumulation of oligosaccharides. When the gsd hepatocytes were incubated in the presence of an inhibitor of alpha-amylase (BAY e 4609) glycogenolysis and the formation of oligosaccharides virtually ceased; the production of glucose plus lactate, already modest in the absence of BAY e 4609, was further decreased by 40%, owing to the suppression of a pathway for glucose production by the successive actions of alpha-amylase and alpha-glucosidase. Evidence was obtained that gsd hepatocytes are more fragile, and that amylolysis of glycogen occurred in damaged cells and/or in the extracellular medium. This may even occur in vivo, since quick-frozen liver samples from anesthetized gsd rats contained severalfold higher concentrations of oligosaccharides than did similar samples from Wistar rats. However, administration of a hepatotoxic agent (CCl4) caused hepatic glycogen depletion in Wistar rats, but not in gsd rats. The administration of phloridzin and of vinblastine, which have been proposed to induce glycogenolysis in the lysosomal system, did not decrease the hepatic glycogen level in gsd rats. Taken together, the data indicate that only the phosphorolytic degradation of glycogen is metabolically important, and that alpha-amylolysis is an indication of an increased fragility of gsd hepatocytes, which becomes prominent when these cells are incubated in vitro.
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PMID:An assessment of the importance of intralysosomal and of alpha-amylolytic glycogenolysis in the liver of normal rats and of rats with a glycogen-storage disease. 387 83

Pancreatic islet cells from pigs (3-12 days old) were maintained in monolayer culture at 37 degrees C for greater than 30 days. Cultures were maintained in enriched Medium 199 with 5% fetal calf serum and with the glucose concentration being cycled between 11.10 and 27.75 mmol/l every 2 days. The presence of B cells in the cultures was demonstrated by insulin secretion into the culture medium, cell staining with aldehyde fuchsin and immunofluorescence. A cells in the cultures were monitored by glucagon secretion into the medium. The absence of exocrine cells was determined by the inability to detect alpha-amylase in the culture medium. Insulin secretion determined over a 34-day period, was found to diminish after 12 days in culture. The fall in levels of extractable B cell insulin with time correlated with the levels of insulin secreted into the medium. Response to short term glucose stimulation (2 h in serum-free medium) was determined on days 6, 10 and 12 in culture. Morphological changes appeared after 25 days in culture, although on day 33 insulin secretion was 62.5 microU X culture-1 X day-1. DNA synthesis (determined by 3H-thymidine incorporation and autoradiography) was demonstrated (day 12, 39.4 +/- 0.9 labelled cells/culture). These findings suggest that pig islet cell monolayer cultures are a useful tool for morphological and biochemical studies and that neonatal pig islets are a potential source of material for transplantation.
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PMID:Monolayer culture of neonatal pig pancreatic islet cells. 634 Nov 46

In order to investigate whether a relationship exists between in vivo insulin secretion and islet mass, 8 patients suffering from severe chronic relapsing pancreatitis were studied before and after pancreatectomy by glucose-glucagon-test (per os 1.75 g glucose; i.v. glucagon 0.01 mg/kg b.w.) and by intravenous glucose-tolerance-test (iGTT) (i.v. glucose 0.33 g/kg b.w.). Postoperative in vitro assessments of pancreatic insulin and alpha-amylase content were performed, and morphometric studies were carried out. Patients were characterized by reduced c-peptide secretion when compared with healthy subjects. The c-peptide response to the glucose-glucagon-test correlated well with the morphometrically estimated exocrine and islet tissue mass (P less than 0.05) and with the content of insulin and amylase in the tissue. The findings suggest that in subjects suffering from severe chronic relapsing pancreatitis the maximal insulin response might represent a parameter for the patient's islet mass.
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PMID:Relationship between insulin secretion and pancreas morphology in subjects with chronic pancreatitis. 639 55

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.
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PMID:Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study. 757 75

A case of a rare pancreatic tumor, duct-acinar-islet cell tumor is presented. The tumor was incidentally found in the pancreatic body on computed tomography of a 21 year old male suffering from mumps. It was well demarcated from surrounding pancreas, and spherical in shape, measured 2.5 cm in diameter. Histologic and immunohistochemical examinations showed the tumor to consist of three distinct cell populations: duct, acinar and islet cells. Small cell nests consisting of these cellular components, either solely of one cell type or mixed of the three cell types, were separated by broad desmoplastic stroma. Islet (endocrine) cells, which were most predominant, were arranged in a trabecular pattern or small cell nests. Most of them were positive for glucagon, and a few cells expressed insulin, somatostatin, serotonin or pancreatic polypeptide. These cells were distributed randomly within the cell nests. Ducts, some of which contained goblet cells, were found among the endocrine cell nests. Duct-islet complexes were also observed. The acinar cells were the least conspicuous component. They expressed pancreatic alpha-amylase. An electron microscopic examination revealed duct cells with intercellular attachments and interdigitations, endocrine cells containing secretory granules, and acinar cells with zymogen granules. No definite evidence suggesting malignancy could be obtained.
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PMID:Duct-acinar-islet cell tumor of the pancreas. 854 40

After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i.v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p < 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (alpha-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (-46%; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mis-matches.
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PMID:Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients. 877 96


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