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)

Gastrin is released by food rich in proteins and by vagal mechanisms. HCI and possibly secretin and glucagon inhibit gastrin release. In the wide range of actions of gastrin, stimulation of gastric acid secretion is the most important. With the advent of radioimmunochemical methods for the determination of gastrinaemia, it has been shown that gastrin exists in a number of forms of different molecular weight. To estimate the validity of gastrin radioimmunoassay it is necessary to demonstrate that decrease in antibody-bound labelled antigen is unrelated to non-specific interference by unknown substances present in serum samples, and that the antiserum reacts with endogenous hormone in an identical manner. Heterogeneity of gastrin in serum may affect the validity of the radioimmunoassay. Hypergastrinaemia associated with hyper-normochlorhydria occures in gastrinoma, hyperplasia of antral gastrin cells, diseases with delayed gastric emptying, retained antrum, short bowel syndrome,renal failure. Hypergastrinaemia associated with hypo-achlorhydria occurs in atrophic gastritis without extensive antral lesion and after vagotomy. Gastrin radioimmunoassay can be used for the mass screening of subjects with atrophic gastritis, a high risk group for gastric cancer.
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PMID:[Gastrin]. 123 74

Histochemical and ultrastructural studies were carried out in four gastric carcinoids, two of which were associated with atrophic gastritis and pernicious anemia. All tumors showed intense argyrophilia and vesicular granules resembling those of endocrine enterochromaffinlike (ECL) cells in normal human gastric mucosa. Tumor cells were found to be unreactive to all the 18 available antiserums to gut hormones, including gastrin, somatostatin, glucagon, and pancreatic polypeptides. The tumors were interpreted as ECL cell argyrophil carcinoids with the various degrees of differentiation and atypia.
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PMID:Gastric carcinoids of argyrophil ECL cells. 723 95

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

The pathomorphological changes in the gastric mucosa and acid production were studied in 118 patients with ulcer disease of a pyloric portion of the stomach and duodenum before and after selective proximal vagotomy in combination with drainage operation. Before the operation, the atrophic changes were the most pronounced in the gastric antrum. Increase in debit of chlorohydric acid was caused by increase in the volume of gastric juice and acid production. Stimulation with food contributes to considerable increase in gastrin concentration in the blood of the patients in low level of glucagon and insulin. Early after the operation, the signs of acute inflammation were revealed in the mucosa of the body and antrum. In increase of a basal level of gastrin and glucagon, acid production significantly decreased. Long-term atrophic gastritis of the body of a stomach was noted mainly in patients with delayed evacuation of its contents. Normalization of the level of hormones correlated with the indices of acid-producing function of the stomach.
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PMID:[Morphological changes and function of gastric and pancreatic mucosa after selective proximal vagotomy in patients with pyloroduodenal ulcer]. 815 39

This review focuses on precursor lesions of gastrointestinal and pancreatic neuroendocrine tumors (GEP-NETs). There are three conditions that are associated with hyperplastic changes in endocrine cells preceding GEP-NETs: autoimmune chronic atrophic gastritis or multiple endocrine neoplasia type 1 (MEN1) with gastric enterochromaffin-like (ECL) cell hyperplasia; MEN1 with gastrin and somatostatin cell hyperplasia in the duodenum and glucagon cell hyperplasia in the islets of the pancreas; and inflammatory bowel disease with endocrine cell hyperplasia in the colon. In gastric ECL cell hyperplasia, it is assumed that hypergastrinemia promotes the growth of the ECL cells of the corpus mucosa and leads to hyperplasia and neoplasia. In the duodenum and the pancreas, the MEN1-associated germline mutation of the menin gene obviously causes hyperplasia of the gastrin and somatostatin cells (duodenum) and the glucagon cells (pancreas), resulting in multifocal development of tumors. These tumors show allelic deletion of the MEN1 gene, whereas the precursor lesions retain their heterozygosity. The endocrine cell hyperplasia in the colon described in inflammatory bowel disease has neither a genetic nor a definite hormonal background.
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PMID:Endocrine precursor lesions of gastroenteropancreatic neuroendocrine tumors. 1805 64

The present study included 104 patients with gastric disorders associated with Helicobacter pylori infection. Thirty of them presented with chronic atrophic gastritis (CAG), 30 with gastric ulcer (GU), 20 with adenomatous gastric polyps (AGP), and 24 with gastric cancer (GC). The control group was comprised of 12 practically healthy subjects. We elucidated the role of vascular endothelial growth factor (VEGF) and endocrine cells of gastric mucosa producing glucagon (GC) and pancreatic polypeptide (PPP) in the patients with GAG, GU, AGP and GC prior to and after the surgical intervention and following eradication therapy. It was shown that GAG, AGP, and GC were associated with the persistence of Helicobacter pylori infection and accompanied by hyperplasia of GC and PPP-secreting endocrine cells of gastric mucosa. GU was characterized by hypolasia of VEGF-secreting epithelial cells of the stomach and GC and PPP-secreting endocrine cells of gastric mucosa. The levels of VEGF, GC and PPP that directly or indirectly realize their pathological properties through H. pylori, Bcl-2, and proapoptotic protein BAX proved to be of high prognostic value as regards the evolvement and clinical course of gastric disorders associated with Helicobacter pylori infection. The study demonstrated that adequate eradication therapy in patients with H. pylori-associated diseases of the stomach significantly reduces the number of gastric cells secreting VEGF and has practically no effect on the amount of GC and PPP-producing endocrine cells of gastric mucosa.
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PMID:[The role of epitheliocytes secreting vascular endothelial growth factor, pancreatic polypeptide and glucagon in the development of oncological diseases of the stomach]. 2264 62