Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Celiac disease is characterized by reversible, gluten-induced, architectural abnormalities of the intestinal mucosa. Villus atrophy is compensated for by an increase in the number of proliferating cells and an increase in crypt cell production rate, resulting in increased crypt length and girth. Several authors, employing various methods of quantitation, have reported enteric endocrine cell hyperplasia in celiac disease. The present study has re-evaluated enteric endocrine cell status in this disorder by employing methods of quantitation which more accurately take account of alterations of crypt morphology than those previously used. Numbers of endocrine cells expressed as cells per unit of crypt length are not increased in the celiac biopsies when contrasted with those from controls. Indeed, numbers of cells immunoreactive for gastrin, GIP, motilin and somatostatin were reduced in the celiac mucosa. Endocrine cell hyperplasia in the celiac small bowel is not as marked as was previously thought, and may lag behind that of the enterocyte population.
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PMID:Reassessment of enteric endocrine cell hyperplasia in celiac disease. 321 24

Chromogranins A and B and secretogranin II have been localized in a wide spectrum of gastroenteropancreatic endocrine/paracrine cells. Chromogranin A immunoreactivity showed the widest distribution and was displayed by glucagon-, PP-, gastrin-, gastrin-CCK-, secretin-immunoreactive cells, the most intense stainings being peculiar of enterochromaffin cells. Chromogranin B immunoreactivity was detected in gastrin- and glucagon cells and in some enterochromaffin cells containing also chromogranin A. Secretogranin II was paired to chromogranin A in glucagon cells of pancreatic islets or occurred alone in glycentin/PP cells of colonic mucosa. Neither of the chromogranins nor secretogranin II have been so far detected in somatostatin-, GIP-, or motilin-immunoreactive cells. Chromogranin A but not chromogranin B or secretogranin II has been detected in the gastric argyrophilic ECL cells.
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PMID:Chromogranins A and B and secretogranin II in hormonally identified endocrine cells of the gut and the pancreas. 322 65

Recent data on the immunolocalization of regulatory peptides and related propeptide sequences in endocrine cells and tumors of the gastrointestinal tract, pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptides are the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, alpha-MSH and CLIP (corticotropin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenaline-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.
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PMID:Endocrine cells producing regulatory peptides. 329 70

The injection of trimebutine induces in the dog an increase of plasma motilin during the fasting period as well as after a meal. We studied the effect of trimebutine on several gastrointestinal hormones released into the circulation by the ingestion of a meal. The intravenous administration of trimebutine (10 mg/kg/h) in 4 dogs abolished the postprandial increase in plasma gastrin, pancreatic polypeptide, insulin, glucagon and GIP. Trimebutine could therefore, by its effects on various regulatory peptides, influence several digestive functions. Its mode of action could probably involves complex mechanisms, including paradoxical effects. The possibility that motilin is a mediator of the trimebutine effect on small bowel smooth muscle is discussed.
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PMID:[Effect of trimebutine on the plasma postprandial release of gastrointestinal hormones in the dog]. 330 10

In a double-blind, crossover study of the effect of ingested medium-chain triglyceride (MCT) and long-chain triglyceride (LCT) in six normal subjects, the gallbladder did not contract after ingestion of MCT but instead had significantly increased in volume at 2 hr after the meal. Plasma cholecystokinin (CCK) increased after the MCT meal, but gastrin, motilin, pancreatic polypeptide (PP), and GIP were unaffected. The long-chain triglyceride meal evoked a brisk and sustained gallbladder contraction, higher levels of CCK, and a significant increase in plasma PP and GIP levels.
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PMID:Comparison of effects of ingested medium- and long-chain triglyceride on gallbladder volume and release of cholecystokinin and other gut peptides. 356 34

It is not known if the increased plasma concentration of noradrenaline in patients with chronic duodenal ulcer disease is a pathogenetic factor or not. The aim of the present study was to investigate if physiologic changes of noradrenaline would evoke any alterations in gastric acid secretion or in the plasma concentration of some gastrointestinal hormones (gastrin, secretin, PP, PYY, and GIP) known to affect gastric physiology. The results show that basal plasma noradrenaline concentration was 1.8 nM and after infusion with noradrenaline at 0.04 or 0.2 nmol/kg/min plasma levels of 2.5 and 4.4 nM were obtained. No appreciable changes could be found in basal or pentagastrin stimulated acid secretion or in any of the gastrointestinal peptides studied. If the elevated plasma noradrenaline concentration observed in duodenal ulcer patients is a pathogenetic factor; it is probable that it interferes with other variables such as blood flow, bicarbonate secretion, or prostaglandin synthesis.
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PMID:Effects of physiological increases of plasma noradrenaline on gastric acid secretion and gastrointestinal hormones. 359 84

In an effort to clarify the effect of pancreatic juice diversion (PJD) on the gastric acid and gut hormone secretion, models of PJD and non-PJD were prepared in dogs with Heidenhain pouch (HP). Two types of operative procedures, pancreatico-jejunostomy with Roux-Y reconstruction as a PJD model (RY group), and pancreatico-jejuno-duodenostomy using interposed jejunum as a non-PJD model (INT group) were carried out. The results were obtained as follows. 1. Both endocrine and exocrine function of the pancreas were preserved by either procedure. 2. Gastric acid secretion from HP after test meal ingestion was significantly increased postoperatively in RY group and was not affected in INT group. 3. Postprandial secretion of gastrin was not affected by these operative procedures in both RY and INT group. Secretion of GIP was significantly suppressed in RY group and was not changed in INT group. Secretion of enteroglucagon was significantly increased in both groups. These results indicate that significant increase of postprandial gastric secretion as shown in RY group is conceivably based on the significant suppression of GIP secretion produced by PJD.
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PMID:[Effect of pancreatic juice diversion on gastric acid and gut hormone secretion]. 369 41

The role of the vagus nerve in the control of gastrin releasing peptide (GRP) stimulated gastroenteropancreatic hormone release and gastric acid secretion was investigated in four conscious gastric fistula dogs using a technique of bilateral cryogenic vagal blockade. A 90-min infusion of GRP at a dose of 400 pmol X kg-1. h-1 produced significant elevations in plasma levels of gastrin, motilin, GIP, enteroglucagon, insulin, pancreatic glucagon, pancreatic polypeptide and VIP. Vagal blockade reversibly inhibited the rise of plasma PP and significantly blunted the elevation of plasma VIP. However, the GRP stimulated response of the other hormones investigated was not modified by vagal blockade. Similarly, the substantial secretion of gastric acid observed with GRP was not influenced by vagal blockade. Thus GRP acts predominantly via mechanisms which are independent of vagal integrity, findings that are in support of a major role for the local neuromodulation of hormone release and gastric acid secretion.
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PMID:The role of vagal integrity in gastrin releasing peptide stimulated gastroenteropancreatic hormone release and gastric acid secretion. 388 1

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding. 389 54

The distribution and quantification of enteroendocrine cells exhibiting immunoreactivities to nine peptides and one amine were examined in the gastrointestinal mucosa of the adult opossum using specific immunocytochemical methods. In the stomach, 90% of the enteroendocrine cells are confined to the pyloric glands and this region contained 73% of the gastrin-containing cells, 60% of the somatostatin-containing cells and 9% of cells reactive for 5-HT. Enteroendocrine cells showing immunoreactivities to glucagon, pancreatic polypeptide, somatostatin and 5-HT were observed scattered within the oxyntic glands. Only somatostatin and 5-HT positive cells were found in the cardiac glands. Immunoreactivities to CCK, glucagon, gastrin, BPP, somatostatin, secretin, motilin, neurotensin, GIP and 5-HT were observed in the epithelium of the small intestine. Although considerable variation exists in the distribution of individual enteroendocrine cell types along the intestinal tract, nearly equal numbers of enteroendocrine cells were observed in each segment. The percentage of enteroendocrine cells increases distally in the colon. Of the three enteroendocrine cell types present, somatostatin- and 5-HT-immunoreactive cells are evenly distributed, whereas neurotensin-immunoreactive cells increase in numbers distally, resulting in an increase in total number.
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PMID:Quantitative distribution of enteroendocrine cells in the gastrointestinal tract of the adult opossum, Didelphis virginiana. 407 99


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