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)

In this study, pyloric stenosis appeared to be a commonly occurring, independent, entity probably resulting from antral pyloric canal gastritis rather than from an ulcer crater per se. An appropriate term might be stenosing pyloritis. Intraoperative effects on the pyloric sphincter from glucagon and atropine administration and stimulation of the vagi and gastric pacemaker were not detectable in a limited study on four cases. A local autonomy of sphincteric action was noted which was not affected by trunkal vagotomy.
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PMID:Pyloric stenosis. 67 66

Side effects of octreotide may be local, biochemical, gastroenterological, or endocrinological. Local pain at the injection site occurs frequently, but rarely lasts more than 15 minutes and often resolves with continued therapy and may be improved if the vial is warmed prior to injection. No long-term hematological or biochemical abnormalities have been described. Despite initial diarrhea in some patients, no change in circulating fat-soluble vitamins has been consistently reported. Antibodies to octreotide have been described, but are rare. Abdominal pain or diarrhea can occur at the beginning of therapy. These symptoms rarely persist and are minimal if the injections are timed between meals, but this may increase the incidence of gallstones. Gallstones occur with increased frequency. Gastritis has been described as being an invariable consequence of long-term treatment with octreotide. We have found the incidence to be increased in patients on octreotide, but this is not invariable. Hypoglycemia may be exacerbated in some patients with insulinoma because of glucagon suppression. Small numbers of patients on octreotide for acromegaly have developed hypoglycemic. Conversely, carbohydrate tolerance may temporarily worsen because of insulin suppression and rarely oral hypoglycemia drug therapy may become necessary. Most frequently, carbohydrate tolerance does not deteriorate. In some patients with acromegaly, pituitary tumor size may continue to increase despite continued therapy. Last, there is the theoretical risk of addiction to a compound which may act through opiate receptors and considerably alleviates headache in some patients with pituitary tumor. Overall, despite the multiplicity of theoretical side effects, the majority of patients tolerate octreotide well, with no serious untoward effects.
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PMID:Proceedings of the discussion, "Tolerability and safety of Sandostatin". 151 39

Insulin, glucagon and C-peptide content in the blood was assayed with the use of commercial radioimmune kits (Diagnostic, USA, and Oris, France). A total of 93 peptic ulcer patients (35 with duodenal peptic ulcer, 28 with gastric ulcer, 16 after Billroth-I resection, and 14 after Billroth-II resection) and 25 patients with chronic gastritis attended by secretory insufficiency were investigated. The study was conducted on empty stomach and after a test breakfast containing 57 g of protein, 63 g of fat, 103 g of carbohydrates that comprised 1212 kcal. The highest changes in hormone incretion were recorded in patients with peptic ulcer disease after Billroth-I and Billroth-II resection, the lowest--in patients with chronic gastritis attended by secretory insufficiency.
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PMID:[Effect of food on blood levels of insulin, glucagon and C-peptide in gastroduodenal pathology]. 162 73

A study was made of changes of the content of hormones (gastrin, insulin, glucagon, triodonthyronine, thyroxine, thyrotrophin, somatotrophin, adrenocorticotrophin and hydrocortisone) under the influence of standard food load in 166 patients with GIT diseases (gastric ulcer, duodenal ulcer, chronic anacid gastritis and chronic enteritis). Forty-three healthy persons entered the control group. Hormones were determined in the peripheral blood by radioimmunoassay. Taking food in healthy persons was shown to cause the stimulation of the secretion of most hormones. To elucidate the mechanisms of hormonal shifts after food load, hormones were also studied after per os intake of solutions with different pH. Disorders of postprandial reactions of the endocrine system which were specific for these nosological forms, were revealed in GIT diseases. The results of the study are of interest in view of new approaches to functional interrelationships of the GIT with endocrine glands.
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PMID:[New approaches to studying the functional relations of the gastrointestinal tract with the endocrine glands]. 408 61

This chapter has covered a wide range of different actions of methylxanthines. They are able to slightly reduce the tone of the lower esophageal sphincter. This is of little concern in the normal individual, but in patients with a reduced initial tone it might lead to heartburn. Coffee intake has been associated with gastritis, but the role of methylxanthines in this effect is obscure. High doses of methylxanthines are also known to be emetic. Practically every function in the intestine can be influenced by high doses of methylxanthines, but the mechanisms involved and the biological significance remain largely obscure. Although in vitro studies with high doses of methylxanthines have demonstrated effects on secretion from salivary glands and exocrine pancreas, there is little evidence that this is clinically important in man. There is also small effects on insulin, glucagon, and TSH secretion. There is a consistent effect on fatty acid mobilization from adipose tissue, which may be of importance, eg, by improving physical performance and by increasing the overall metabolic rate. There is also some evidence for long-term effects on fat depots. By contrast, the effects on carbohydrate metabolism are much less prominent and reproducible, and may to some extent be secondary to altered lipid metabolism. Despite more than a century of effort to elucidate the actions of methylxanthines in man, one of the major conclusions to be drawn is that there is a need for further studies. In view of the newer ideas about the mechanism of action of caffeine and other methylxanthines, careful studies, especially of long-term effects of methylxanthines on several aspects of gastrointestinal function, on calcium homeostasis, on body composition, and on physical performance, would be desirable.
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PMID:Gastrointestinal and metabolic effects of methylxanthines. 608 44

A 19-yr-old male developed severe hemorrhagic gastritis following three abdominal operations. Treatment with intravenous cimetidine and hourly antacids to maintain his gastric pH above 5 failed to affect gastrointestinal bleeding. Also, peripheral venous vasopressin, propantheline bromide, and glucagon were without effect. Total gastrectomy was considered to control his bleeding. However, since a number of prostaglandin analogs prevent gastric lesions produced by many noxious agents (e.g., aspirin, alcohol, strong acid or alkali, etc.) in animals and humans, the patient was treated with 50 micrograms of 15(R)-15 methyl prostaglandin E2 intragastrically every 6 h for 10 days. To epimerize the 15(R) form to the more active 15(S) form, 50-100 ml of 50-mN HCl was placed into the patient's stomach immediately before each dose. Bleeding ceased within 24 h of the onset of 15(R)-15 methyl prostaglandin E2 therapy and did not recur. The prompt response to 15(R)-15 methyl prostaglandin E2 in combination with hourly antacids in this patient with persistent and severe hemorrhagic gastritis suggests a therapeutic effect and the need for a prospective double-blind clinical trial.
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PMID:Treatment of hemorrhagic gastritis with 15(R)-15 methyl prostaglandin E2: report of a case. 697 84

The blood serum content of secretin, vasointestinal peptide (VIP), glucagon and insulin was studied in 112 patients with chronic gastritis presenting with secretory deficiency, and 12 essentially healthy subjects. It was established that in surface, fundal and pangastritis the levels of secretin and VIP did not differ from the values in healthy individuals. The secretin concentration tended to be the lowest in atrophic fundal and atrophic pangastritis. They also had significantly elevated concentrations of VIP and glucagon, with insulin decreased. Caused by different exo- and endogenous factors phenomena characteristic of gastritis, such as disturbances in acid-producing function of the stomach, to mention but one of its manifestations, result in changes of stimulatory effects of acidification on enterinic elements of the small intestine, which circumstance leads to discoordination in output of intestinal and pancreatic hormones particularly pronounced in atrophic gastritis.
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PMID:[Enteroinsular hormones in chronic gastritis with secretory insufficiency]. 748 47

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

Fasting and postprandial plasma levels of the gut hormones gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide, motilin, neurotensin, peptide YY (PYY), enteroglucagon, glucagon, insulin, and pancreatic polypeptide were measured in 11 patients with alkaline gastritis associated with excessive duodenogastric reflux not related to previous gastric surgery (primary DGR), 12 primary DGR patients after pancreatico-biliary diversion ("duodenal switch" procedure), and in 10 age-matched healthy controls. Gastric emptying of a semisolid oatmeal was also measured in patients with primary DGR and in patients after bile diversion. Fasting plasma levels of the distal gut hormone neurotensin and the pancreatic islet hormone insulin were significantly greater in patients with primary DGR compared with controls. Neurotensin levels were normal in patients studied after bile diversion. Postprandial plasma levels, incremental integrated and total integrated responses for CCK, secretin, insulin, neurotensin, PYY, and enteroglucagon, were significantly greater in patients with primary DGR compared with controls. The majority of these responses normalized after bile diversion; however, the postprandial response for insulin and enteroglucagon remained elevated. Patients with primary DGR had a rapid early postprandial phase of gastric emptying of solids, which showed a significant correlation with plasma neurotensin levels. Bile diversion produced a significant delay in this lag-phase of gastric emptying. These abnormalities in gut regulatory hormones appear to be adaptive changes to rapid early postprandial gastric emptying, probably related to antropyloric dysmotility, which has been implicated in the pathogenesis of this condition. Measurement of these gastrointestinal hormones may become useful in the diagnosis of primary DGR.
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PMID:Abnormal plasma gut hormones in pathologic duodenogastric reflux and their response to surgery. 841 94

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22


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