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)

Manometric study was performed to compare the inhibitory effect of glucagon and secretin on the gastroduodenal motor activity by infused catheter method. The subjects consisted of 3 healthy volunteers and 7 patients with peptic ulcer and other diseases. The following results were obtained. After the intravenous administration of glucagon (1 mg), the motor activity of the stomach and duodenum was inhibited promptly. According to statistic evaluation, the contraction numbers and motility index decreased significantly during 25 minutes compared with the basal values in both stomach and duodenum. After the administration of secretin (100 units), gastric motor activity was markedly inhibited, although duodenal motility increased during 10 minutes due to the initiation of secretin-induced migrating motor complex. The contraction numbers and motility index in stomach decreased significantly during 20 minutes after the administration. The inhibitory effect of glucagon was more remarkable in duodenum than in stomach. On the other hand, secretin was more effective in stomach than in duodenum.
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PMID:[Comparative study on the inhibitory effect of glucagon and secretin on the gastroduodenal motility in man]. 653 71

A patient is described who presented with a 10 year history of intermittent peptic ulcer symptoms and a 3 year history of an undiagnosed skin rash. Investigations indicated raised plasma levels of gastrin, glucagon and pancreatic polypeptide. A single tumour was localised to the pancreas and resected. The tumour had the typical histology of an apudoma, and contained cells which stained for gastrin, glucagon, pancreatic polypeptide and neurotensin.
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PMID:A unique apudoma producing the glucagonoma and gastrinoma syndromes. 687 3

Physiological regulatory mechanisms of gastric acid secretion are the basis for all those studies which attempt to analyze the pathophysiological role of acid secretion. The major stimulus of parietal cell function is food intake which acts via activation of cephalic-vagal and gastric mechanisms. Cephalic phase of acid secretion is augmented predominantly by acetylcholine and gastrin while histamine is of major importance during the gastric phase. A contribution of neuropeptides located in the ex- and intrinsic nervous system such as enkephalin, beta-endorphin, gastrin-releasing peptide and neuromedin C ist most likely, however, their exact physiological role remains to be determined especially in man. Following maximal acid secretion parietal cell function is turned down which is paralleled by the decrease of intragastric pH. The mechanisms responsible for this effect originate in the stomach and small intestine. In contrast to the stimulatory factors the physiologically relevant inhibitors of acid secretion are less well known. Hormones such as somatostatin, glucagon-like peptide-1 (7-36)-NH2 and peptide YY are presumably of importance. The role of secretin, GIP, CCK and neurotensin is somewhat more controversial and remains to be examined in greater detail in humans. Especially the synergistic action of gastrointestinal hormones is virtually unknown. The increasing knowledge of the complex regulatory mechanisms in the stomach should result in new perspectives for the pathogenesis of peptic ulcer disease.
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PMID:[Physiologic regulation of gastric acid secretion]. 847 47

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

We report the case of a 49-yr-old man affected by coma and hypoglycemia unawareness following repetitive hypoglycemic episodes due to dumping syndrome. The dumping syndrome, which was due to partial gastrectomy and vagotomy performed for recurrent peptic ulcer, was responsible for reactive hyperinsulinemia as demonstrated by an oral glucose tolerance test. While the glucose counterregulatory hormones were all normally sensitive to specific stimulation tests, insulin-induced hypoglycemia failed to induce an adequate counterregulatory response, causing no response in plasma norepinephrine, a slight and short increase in plasma cortisol, ACTH and glucagon and an insufficient increase in plasma epinephrine and GH. This case demonstrates that hypoglycemia unawareness has to be taken into account not only in patients affected by IDDM or insulinoma but also in any case of reactive hypoglycemia.
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PMID:Hypoglycemia unawareness in a patient with dumping syndrome: report of a case. 976 63

Glucagon suppresses gastric acid secretion in normal subjects and in ulcer patients. It has no inhibitory effect while the stomach is under maximal histamine stimulation. The mechanism of action is discussed, and experiments are described which indicate that glucagon is unlikely to be of value in the treatment of peptic ulcer.
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PMID:Effect of Glucagon on Gastric Secretion in Man. 1866 31


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