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)

After an acute episode of pancreatitis, a 63-year-old man was found to have a pancreatic glucagonoma. The tumor was resected without evidence of metastases. Three years later he had symptoms of uncontrolled diabetes, no skin lesions, and diarrhea and was found to have a pancreatic pseudocyst and multiple hepatic metastases. Glucagon concentrations were raised but were suppressible by glucose and somatostatin and responded to arginine stimulation. He was treated for 6 months with octreotide (Sandostatin), which reduced his symptoms; the pseudocyst resolved, but liver metastases continued to grow. Although spontaneous resolution of the pseudocyst is possible, this case appears to illustrate differences in sensitivity of endocrine and exocrine tissues to suppression by Sandostatin.
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PMID:Somatostatin analogue in treatment of coexisting glucagonoma and pancreatic pseudocyst: dissociation of responses. 216 87

Findings of dynamic cholangiomanometry with the analysis of the tension curves are overviewed. This technique helped reveal different functional ailments of the bile papilla in major variants of the cholelithiasis course (acute obstructive++ cholecystitis, recurrent pancreatitis, and choledocholythiasis with obstructive jaundice). Parallel radioimmunoassay-based studies of a series of gastrointestinal polypeptides (insulin, glucagon, gastrin, vasoactive peptide, bombesin , and somatostatin) were conducted to determine the importance of these polypeptides in the pathogenesis of cholelithiasis complications. The levels of certain polypeptides were found to be related to the clinical manifestations of the disease. The complex assessment of the bile papilla function and gastrointestinal polypeptide concentrations offers a possibility for elaborating the pathogenetically relevant methods of therapy for this group of diseases.
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PMID:[Plasma levels of various gastrointestinal polypeptides in patients with cholelithiasis and different degree of functional disorders of the major duodenal papilla]. 227 84

In this review, we compared the outcome of 25 studies of experimentally induced pancreatitis in animals with 13 studies of human acute pancreatitis in which the same therapeutic agents were used (aprotinin, glucagon, 5-fluorouracil, somatostatin, peritoneal lavage). Whereas 81% of the animal studies had a positive outcome (improvement in survival), only 7.7% of the human studies showed a positive outcome on survival. Most animal studies suffered from a protocol in which treatment was not significantly delayed after induction of acute pancreatitis. Of the 12 human studies that showed no effect of treatment on survival, none had sufficient statistical power (1 - beta error) for the investigators to have confidence in the negative outcomes. This was due to the fact that the studies had too few patients or that the event rates in the untreated populations were too low. Only five of the human studies reported the complication rates of acute pancreatitis in patients who did not die of their disease. Treatment (by any agent) did not improve the complication rate in these studies, but only one of the five reports had sufficient statistical power for the investigators to have confidence in these negative results. Large multicenter studies with sufficient numbers of patients with severe pancreatitis (high mortality and complication rates) are needed to evaluate new therapies in this disease.
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PMID:Treatment of acute pancreatitis. Comparison of animal and human studies. 244 20

Somatostatin is an inhibitory hormone that decreases the secretion and end organ response of cholecystokinin (CCK). Inhibition of hormonal stimulation of pancreatic exocrine secretion by somatostatin may improve the course of acute pancreatitis. Anesthetized dogs underwent cholecystectomy and cannulation of the pancreatic duct, thoracic duct, and portal vein. Twenty experiments were performed in random order with 5 dogs in each group. Hourly measurements of lymph flow and portal and thoracic duct amylase were made. Portal blood insulin, glucagon, and CCK concentrations were determined by radioimmunoassay on samples obtained at the beginning and end of the experiments. Pancreatitis was induced by injecting, under constant pressure, 10 ml bile into the pancreatic duct during 1 min. Somatostatin was administered intravenously (20 micrograms/kg/hr). After 5 h, the dogs were killed, pancreas glands removed and weighed and tissue samples obtained for histologic evaluation. There was a significant increase in lymph amylase output and portal venous amylase and CCK concentrations in the dogs with pancreatitis compared to the control dogs. In dogs with pancreatitis, lymphatic amylase secretion and portal CCK concentrations were significantly decreased by somatostatin. Somatostatin did not significantly alter portal amylase concentrations, pancreas gland weights or histologic inflammation when compared to values from dogs with pancreatitis not treated with somatostatin.
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PMID:Effects of somatostatin on acute canine experimental pancreatitis. 244 77

The ability of atrial natriuretic peptide (ANP) to preserve renal function in dogs with hypovolemic acute renal insufficiency was tested in anesthetized dogs 4 h after the induction of acute pancreatitis. Plasma volume had decreased by 21.5% and glomerular filtration rate (GFR) by 43.2%. Blood pressure had declined by 30 mmHg. ANP was given intravenously at 50 and 150 ng.kg-1.min-1. With the lower dose, blood pressure (BP), GFR, and clearance of p-aminohippuric acid (CPAH) did not change but urine flow (V) and sodium excretion (UNaV) increased. With the higher dose, BP declined by 25 mmHg, GFR declined, but V and UNaV still increased. When plasma volume was maintained with 4% colloid during the progression of pancreatitis and ANP 50 ng.kg-1.min-1 given, BP declined, GFR did not change, and there was a magnified increment in V and UNaV. The administration of glucagon (5 micrograms/min iv) to dogs with hypovolemic pancreatitis caused BP to decline by 17 mmHg. Despite a major increment in GFR, fractional excretion of sodium increased only slightly, compared with that obtained with ANP. We conclude that glucagon preserves GFR more effectively than ANP in hypovolemia, but ANP is more effective in protecting urinary water and sodium excretion.
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PMID:Response to atrial natriuretic peptide in dogs with hypovolemic acute pancreatitis. 252 75

The effect of complete Freund's adjuvant (CFA), in combination with streptozotocin (STZ), on pancreatic insulin content, plasma glucose, and pancreatic histopathology were studied in male Balb/c mice. One injection of CFA, followed 24 h later by a single dose of 100 mg/kg of STZ (group I), produced a 92% (p less than 0.01) reduction in pancreatic insulin, a 54% (p less than 0.01) increase in glucagon content, and severe hyperglycemia. The depletion of pancreatic insulin was associated with degranulation, necrosis of beta cells, and reduction of the apparent islet size. Focal pancreatitis, without apparent islet inflammation, occurred in all animals in this group. After treatment with STZ alone (group II), pancreatic insulin content decreased 73% (p less than 0.01), whereas plasma glucose levels, even though being in the hyperglycemic range, were significantly lower (p less than 0.02) than the mice in group I. Although pyknotic and hypertrophic cell nuclei could be observed in several islets of mice from group II, major histopathological changes, such as pancreatitis and extensive beta cell necrosis seen in group I, were absent. The results show that in the Balb/c mouse strain, a nonspecific insult by CFA prior to a cell-specific cytotoxic insult markedly enhanced destruction of beta cells and the development of hyperglycemia.
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PMID:Augmentation of streptozotocin-induced hyperglycemia in mice by prior treatment with complete Freund's adjuvant. 252 77

The tropical calcifying pancreatitis and/or fibrous pancreatitis are responsible for a number of cases of juvenile insulin-dependent diabetes in the Third World countries. World wide distributed in the tropical areas of Asia, Africa and South America, they can also be observed in Europe, in migrants from these countries. Intensive epidemiological and biochemical studies are currently developed in order to shed light on the many obscure points. Classification of the typical calcifying pancreatitis and the related syndromes is a matter of debate. The pathological basis is calcification of the pancreas and echography of the gland may become a cheap convenient relatively specific tool for epidemiology. The clinical syndrome consists of chronic painful pancreatic episodes since childhood, associated with pancreatic exocrine insufficiency, followed by the onset, during adolescence, of diabetes mellitus, which is most of the times insulin dependent. Patients' history is free of chronic alcoholism, but includes constantly chronic caloric and proteic malnutrition. Although insulin dependent this diabetes in not prone to ketosis, due presumably to carnitine deficiency and relative glucagon deficiency (or suppressibility). Insulin resistance is traditionally noted, the pathophysiology of which is unknown. The mechanism of calcification appearance is also undetermined. Either a deficiency in pancreatic stone protein, or the toxic effect of cyanogen glucosides present in cassava and other tropical foodstuffs, or the malnutrition-related deficiency in sulphur-containing aminoacids may be causal factors. No valid experimental model of the disease is available.
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PMID:[Diabetogenic tropical pancreatitis]. 304 66

A total of 32 histologically documented cases of heterotopic pancreas was found in a review of the records of the department of pathology at the Chang Gung Memorial Hospital between 1977 and 1987. This review was done to ascertain the clinical significance of this uncommon entity. In 14 patients (44%), the aberrant pancreatic tissue was symptomatic; in the other 18 (56%), it was found incidentally. In the symptomatic group, the heterotopic pancreatic tissue was found in a duplication cyst of the ileum in one patient, in the common bile duct in one, in a Meckel's diverticulum in four, in the stomach in three, in a congenital duodenal diaphragm in one, in the duodenum in three, and in the ileum in one. The majority of heterotopic pancreatic tissue in the asymptomatic group was encountered in the jejunum (15 patients). Symptoms were related to complications, including obstruction of the common bile duct, mucosal ulcer with hemorrhage, intussusception, and intestinal obstruction, but not to pathologic conditions of the pancreas itself, such as pancreatitis or pancreatic cyst or neoplasm. In all of the clinically significant cases, the clinical symptoms disappeared completely after surgical removal of the aberrant tissue. In 28 cases (87%), diagnosis was made by frozen section during operation. Preoperative diagnosis of aberrant pancreas was not made in any of the cases. Histologically, all cases showed pancreatic excretory ducts; in 31 cases (97%), exocrine glands were present, and in 27 cases (84%), islets of Langerhans were discernible. There was no relationship between symptoms and the presence of islets, acini, or ducts. Mallory's phosphotungstic acid-hematoxylin stain was used to demonstrate zymogen granules in the acinar cells, and insulin, glucagon, and somatostatin were demonstrated with the horseradish peroxidase-antihorseradish peroxidase immunocytochemical staining technique; islets of Langerhans were also identified. Technetium Tc 99m scintigraphy was used to detect the bleeding source in a Meckel's diverticulum and an enteric duplication associated with ectopic gastric mucosa.
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PMID:Pancreatic heterotopia: a reappraisal and clinicopathologic analysis of 32 cases. 305 29

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p less than 0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a "multistep" process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.
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PMID:Aberrant expression of class II major histocompatibility complex molecules by B cells and hyperexpression of class I major histocompatibility complex molecules by insulin containing islets in type 1 (insulin-dependent) diabetes mellitus. 330 84

The experiments on normal mongrel dogs and those with chronic experimental pancreatitis were performed to reveal the early changes of the endocrine pancreas function. The concentration of immunoreactive insulin and glucagon were studied in afferent vessels of the organ after intraarterial glucose-loading during pancreatic perfusion in situ. The data obtained have shown that in chronic pancreatitis the maximum secretion of insulin is decreased and delayed, as compared to normal animals. At the same time insulin-glucagon secretion ratio remains unchanged. That was indicative of the normal alpha-cell function at the early stages of the disease.
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PMID:[Characteristics of endocrine disorders in the early stages of the development of chronic experimental pancreatitis]. 331 35


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