Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhoea is a common gastrointestinal disorder which is a state of fluid and ion loss from the gut. Cauvery-100, an Ayurvedic formulation has been used in this study for the treatment of diarrhoea. Diarrhoea was induced in experimental rats by oral administration of castor oil. The increased gastrointestinal motility in diarrhoea was brought back to near normal levels on the treatment of Cauvery-100. The activities of the enzymes alkaline phosphatase, total ATPase and Na+,K(+)-ATPase were decreased in the diarrhoeal group and was brought back to near normal levels in the treated group. The serum levels of sodium and potassium were decreased in the diarrhoeal group and brought back to normal levels in the treated group. Prior treatment of the drug Cauvery-100 did not induce diarrhoea on administration of castor oil, suggesting the protective influence of the drug on the gastrointestinal tract.
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PMID:Biochemical studies on the antidiarrhoeal effects of Cauvery-100, an ayurvedic formulation, in rats. 166 70

We tested the hypothesis that the gastric H+/K+ adenosine triphosphatase inhibitor, omeprazole, because of its different mode of action and pronounced inhibitory effect on gastric acid secretion, may be more effective in peptic ulcer that is refractory to histamine H2 receptor antagonist treatment than continuing the same therapy. Altogether 107 patients (duodenal ulcer, n = 88; prepyloric ulcer, n = 14; gastric ulcer, n = 3; mixed sites, n = 2) with refractory peptic ulcer - that is ulcer unhealed after at least two months' treatment with cimetidine 0.8 g or 1 g daily or with ranitidine 0.3 g daily - were randomly allocated to receive either omeprazole 40 mg daily (n = 54) or to continue treatment with the same H2 receptor antagonist and at the same dose (n = 53) for up to eight weeks. The patients in the two treatment groups were well matched demographically. Healing by 'intent to treat' analysis was as follows: at four weeks, omeprazole 46 of 54 (85%), H2 receptor antagonist 18 of 53 (34%) (p less than 0.0001); and at eight weeks, 52 of 54 (96%) and 30 of 53 (57%) respectively (p less than 0.0001). One patient was lost to follow up but of the 22 patients whose ulcers were shown to be unhealed at endoscopy after receiving continued H2 receptor antagonist treatment, 21 healed in four to eight weeks when changed to omeprazole. Daytime epigastric pain cleared at four weeks in 43 of 47 (91%) patients on omeprazole and in 32 of 46 (70%) on H2 receptor antagonists (p=0.01) and relief of all dyspeptic symptoms occurred in 39 of 47 (83%) and 23 of 45 (51%) (p=0.0009) patients respectively. Adverse events occurred in 11 of 54 (20%) patients on omeprazole and in 12 of 35 (34%) on cimetidine but in none on ranitidine. The events were mild and none required treatment withdrawal. The commonest event in patients on omeprazole was loose stools or diarrhoea (n=5). Omeprazole was significantly better than continued H2 receptor antagonist treatment for the short term management of refractory peptic ulcer as judged by healing rate and pain relief, and it was safe.
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PMID:Treatment of refractory peptic ulcer with omeprazole or continued H2 receptor antagonists: a controlled clinical trial. 162 76

Several alterations of the small-intestinal morphology and function have been documented after alcohol ingestion. There are morphologic changes macroscopically and microscopically after acute alcohol administration in the proximal part of the small intestine, which are quickly reversible. There are no macroscopic changes and, in most patients, very discrete light microscopic changes in the small intestine after chronic alcohol ingestion. The ultrastructural changes are, however, profound, as seen by both transmission and scanning electron microscopy. The permeability is probably increased, permitting entrance of possible noxious agents, which may explain some of the extraintestinal tissue damage observed in chronic alcoholism. The transit is increased, at least after acute alcohol administration, perhaps contributing to the diarrhea commonly seen after heavy drinking. Several of the enzymes located in the brush border are affected; lactase activity can be depressed and perhaps result in a transient milk intolerance in predisposed individuals. The activity of GGT is increased and may partly account for the GGT elevation in serum after heavy drinking. Other enzymes, such as Na(+)-K(+)-ATPase, can be inhibited and result in a decreased absorption of substances that require active, energy-dependent transport mechanisms. The secretion of water and electrolytes may be increased (an effect on cAMP?). The absorption of several nutrients, vitamins, and other elements is disturbed. The bacterial flora is increased and changed, which may give rise to symptoms and also increase the production of acetaldehyde by bacterial metabolism of ethanol. Acetaldehyde is more toxic than ethanol, and an increased concentration of acetaldehyde can possibly accentuate the damage to the liver and other organs. The bacterial overgrowth can possibly cause endotoxinemia. Although studies on alcohol-related intestinal alterations have been relatively sparse, the acute and chronic effects of alcohol thus seem to be considerable. From available results it is, however, difficult to draw any definite conclusions about the clinical importance of many of the findings. Future research will need to study the relationship between, for example, the chronic morphologic changes, the absorptive dysfunction, and permeability alterations, on the one hand, and the gastrointestinal symptoms, the extraintestinal damage, and various deficiencies, on the other hand.
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PMID:Alcohol and the small intestine. 200 95

As clinical experience with patients with ZES has grown, increasing recognition has been made of the broad spectrum of symptoms associated with gastrinomas. Diarrhea and acid-induced esophageal injury have taken their place alongside chronic peptic ulcer disease as indications for screening for gastrinoma. Diagnostic testing should begin with fasting serum gastrin levels and should include intravenous secretin infusion if fasting serum levels of gastrin are nondiagnostic and the patient is not found to be hypochlorhydric. Tumor localization is critical to aid in the identification of patients with potentially curable localized disease. Preoperative evaluation utilizing CT scanning with intravenous contrast should be done early and should be supplemented by other imaging modalities as necessary. Exploratory laparotomy, including a thorough examination of the duodenum and perhaps intraoperative ultrasound, should be performed in all patients with sporadic gastrinoma who lack evidence of extensive metastatic disease on preoperative evaluation. By utilizing this approach, it is likely that at least 20% of patients with ZES can be cured. With the availability of the highly effective H(+)-K(+)-ATPase inhibitor omeprazole, excellent control of symptoms related to gastric acid hypersecretion can be expected. Patients with unresectable gastrinoma may thus avoid potentially morbid antisecretory surgery and be managed with a fairly simple medical regimen. Further developments in the chemotherapeutic management of these patients with unresectable disease should be forthcoming in the future.
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PMID:Zollinger-Ellison syndrome. 207 95

Several studies pointed out an altered stool pattern as the most common side effect of auranofin therapy. The major mechanism in the aetiology of auranofin-induced impairment in bowel habit seems to be the inhibition of Na+/K+ ATPase in the gut. In vitro experiments proved that auranofin can affect active bile acid (BA) reabsorption in rat terminal ileum; this action, due to the ability of the drug to reduce Na+ pump activity by inhibiting Na+/K+ ATPase, may make a significant contribution to the auranofin-induced diarrhoea. The ability of auranofin to reduce the Na+ gradient necessary for active BA reabsorption, however, could cause a decrease of serum BA levels in patients taking auranofin before or without the development of an overt diarrhoea. We measured fasting and postprandial serum conjugated BA levels in 10 female rheumatoid arthritis patients before and after one month and two months' auranofin treatment. No patient developed diarrhoea during the chrysotherapy. When oral gold salt therapy was started, we observed a slight decrease in serum BA levels, but difference was not statistically significant. We can conclude that auranofin therapy does not cause BA malabsorption in patients who do not develop diarrhoea during the treatment.
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PMID:Effect of oral gold salt therapy on bile acid absorption in rheumatoid arthritis patients. 233 51

To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age. The suckling rat was approximately 50 times more sensitive to CT in triggering the secretory response than the weaned rat, when estimated by the medium-effective dose (ED50, 0.8 vs. 38.9 nM). Cortisone, known to promote enterocyte maturation, when injected into suckling rats, decreased host sensitivity approximately 1,000 times. Neither age nor cortisone decreased the receptor binding of 125I-labeled CT to intestinal microvillus membranes. In contrast, cortisone treatment caused a threefold increase in receptor density from 14.5 to 43.0 pmol/mg protein. The enzyme responsible for the sodium pump, Na+-K+-ATPase, showed a threefold increase in activity both after weaning and after a cortisone treatment. These data indicate that the immature gut exhibited an increased host sensitivity to CT stimulation that was not correlated with initial receptor binding but was related to a lowered Na+-K+-ATPase activity, suggesting that an underdeveloped sodium pump may be partially responsible for the high incidence of secretory diarrhea in neonates.
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PMID:Age and cortisone alter host responsiveness to cholera toxin in the developing gut. 253 37

Activity of alkaline phosphatase (apical membrane) and Na+, K+-ATPase (basal membrane) is determined to decrease in the membrane fractions of intestinal epithelium in the diarrheic new born cattle. It is concluded that Na+, K+-ATPase of basal membranes play a fundamental role in Na+ loss by body with diarrhea.
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PMID:[Changes in the activity of alkaline phosphatase and Na K ATPase in the membrane fractions of small-intestinal epithelium in the normal state and in diarrhea]. 254 66

The effects of intestinal resection on several intestinal parameters have been studied in the large intestine of rats one month after the surgical operation. The results show that both 50% and 80% distal small bowel resection increased net fluid absorption and mucosal permeability and caused expansion of the intercellular spaces of the large intestine. The increase in net fluid absorption was dependent upon the extent of the intestine removed. The cAMP and cGMP content of cecal and colonic mucosa were significantly reduced after jejunoilectomy. Changes in nucleotide levels were dependent on the length of the intestine resected. On the other hand, mucosa Na,K-ATPase specific activity was only increased in the cecum after 80% intestinal resection. The results are discussed in terms of adaptation to prevent diarrhea.
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PMID:Role of rat large intestine in reducing diarrhea after 50% or 80% distal small bowel resection. 255 20

Mucosal Na,K-ATPase activity was studied in rectal biopsy specimens from 19 children with ulcerative colitis (UC) (mean age, 13 years) and 4 children with Crohn's colitis (mean age, 14 years) and compared with biopsy specimens from 12 control children (mean age, 12 years). The Na,K-ATPase activity was significantly decreased in UC with severe rectal inflammation compared with UC in remission or with children with unspecific symptoms and normal mucosa (p less than 0.001, respectively). A higher enzyme activity was shown with age in the group with normal rectal mucosa and no evidence of inflammatory bowel disease (n = 17). The decreased Na,K-ATPase in UC with severe rectal inflammation might contribute to the diarrhoea by impairment of sodium transport.
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PMID:Na,K-ATPase activity in rectal mucosa of children with ulcerative colitis and Crohn's disease. 255 82

We measured the effect of pharmacological doses of glucocorticoid on piglet jejunal structure and function during acute viral diarrhea. Weaned piglets, infected experimentally with transmissible gastroenteritis virus, a coronavirus that induces a diarrheal illness similar to human rotavirus infection, received methylprednisolone (30 mg/kg) or saline intramuscularly at 48 and 72 h after infection; noninfected littermate controls were similarly injected with methylprednisolone. Animals were killed at 96 h, at the height of diarrhea, and jejunal epithelium was studied in vitro. Transmissible gastroenteritis, as expected, induced structural, enzyme, and Na transport abnormalities. Methylprednisolone did not affect small intestinal structure or function of noninfected control piglets. In transmissible gastroenteritis-infected piglets, jejunal villi were longer and glucose-facilitated Na absorption was greater after methylprednisolone than after saline treatment. Increased glucose stimulation of Na flux in vitro in the methylprednisolone-treated infected group was not attributable to enhanced Na+-K+-ATPase activity and occurred despite persistence of the virus within mucosal cells, shown by immunofluorescence microscopy. In this piglet model of viral diarrhea, early regeneration of absorptive surface that precedes recovery of disaccharidase function is accelerated by glucocorticoid therapy.
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PMID:Effect of glucocorticoid on piglet jejunal mucosa during acute viral enteritis. 283 16


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