Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To better understand the pathogenesis of infantile viral gastroenteritis, we studied Na+ and Cl- fluxes in vitro in short-circuited jejunal epithelium from 8-10-day-old piglets after infection with a standard dose of human rotavirus given via nasogastric tube. 11 infected piglets, all of whom became ill, were compared with 9 uninfected, healthy litter-mates. When killed 72 h after infection, intestinal villi were shorter and crypts deeper (P less than 0.025) in duodenum, upper jejunum, and mid-small intestine, but not ileum in infected piglets. Virus antigen was seen by fluorescence microscopy in occasional jejunal villus tip cells in only four infected piglets and no controls at 72 h. Net Na+ and Cl- fluxes did not differ from noninfected litter-mate controls under basal conditions, but response to glucose was blunted in infected piglets (P less than 0.001). Theophylline stimulated net Cl- secretion in both infected and control animals, and cyclic AMP concentration in isolated jejunal villus enterocytes did not differ significantly. In isolated jejunal villus enterocytes of infected piglets, thymidine kinase activity increased (P less than 0.001), and sucrase activity decreased (P less than 0.001). We conclude that in this invasive enteritis caused by a major human viral pathogen, glucose-coupled Na+ transport is impaired in the jejunum at a time when the villus epithelium shows enzyme characteristics of crypt epithelium, and when little or no virus is present. These findings are identical to those occurring in an invasive coronavirus enteritis of piglets but differ markedly from those seen with enterotoxigenic diarrhea.
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PMID:Human rotavirus enteritis induced in conventional piglets. Intestinal structure and transport. 19 22

1. Stimulation of fluid secretion from fly salivary glands by 5-hydroxytryptamine (5-HT) is known to involve calcium and cyclic AMP. Isolated salivary glands were used to investigate the role of these second messengers in the control of enzyme (sucrase) secretion.2. The protein component of secretion from isolated glands treated with 5-HT appears to be identical to that of saliva secreted by flies during feeding.3. Stimulation of fluid secretion by 5-HT follows a definite dose-response curve, but there is no consistent relationship between the rate of enzyme secretion and the stimulating concentration of 5-HT.4. Exogenous cyclic AMP causes secretion of enzymes as well as of fluid, thus mimicking the action of 5-HT. The phosphodiesterase inhibitor theophylline enhances the rate of 5-HT-stimulated enzyme secretion.5. Removal of calcium from the bathing medium enhances enzyme secretion in response to 5 or 10 nM-5-HT but has no effect on enzyme secretion stimulated by 100 nM-5-HT or by cyclic AMP.6. Addition of 0.1 mM-lanthanum to medium containing 2 mM-calcium mimics the effect of calcium-free solution on 5-HT-stimulated enzyme secretion.7. The ionophore A 23187 causes secretion of both fluid and enzyme. The secretory rate is initially high but soon declines and ceases after about 40 min.8. Enzyme secretion in response to 5-HT or to cyclic AMP is progressively inhibited as the concentration of potassium is increased from 10 to 80 mM. Secretion in response to A 23187 is initially inhibited by 80 mM-potassium but then partially recovers.9. The rate of enzyme secretion appears to be affected by the intracellular concentrations of both calcium and cyclic AMP. It is possible that the rate of enzyme secretion increases as the intracellular calcium concentration rises, until the optimal calcium concentration is reached when further increase in the level of calcium progressively inhibits secretion. The optimal calcium concentration for enzyme secretion is lower than that for fluid secretion, and 5-HT normally causes maximal fluid secretion and submaximal enzyme secretion.
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PMID:The control of enzyme secretion from fly salivary glands. 20 76

The rat small bowel was perfused in vivo and ex vivo in the absence of biliary and pancreatic secretion. Intraluminal release of sucrase, alkaline phosphatase, aminopeptidases and enterokinase was significantly increased after administration of pentagastrin, caerulein and glucagon at doses ranging between 1 pg and 10 microgram. This suggests that there is a direct hormonal stimulation of the intestinal mucosa. This effect might at least partly be mediated through cyclic AMP since dibutyryl derivates of this cyclic nucleotide exerted a significant stimulatory effect on intraluminal release of proteins, sucrase and enterokinase, although the pattern of enzyme was quite different from the effect produced by the three peptides.
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PMID:Hormonal stimulation of intestinal brush border enzymes release. 20 30

The uptake of macromolecular markers by fluid pinocytosis in the rat yolk sac was inhibited by glucagon, with half-maximal effect at a hormone concentration of approximately 3 X 10(-8) M. Glucagon had no effect on the cellular distribution of the marker subsequent to its uptake. Rates of uptake promptly returned to normal when the yolk sacs were transferred from a glucagon-containing to a glucagon-free medium. Epinephrine also inhibited, but only at much higher concentrations. The effect of the latter was augmented by theophylline. Insulin (10(-6) M) had no effect when added alone or with an inhibitory level of glucagon (10(-7) M). The presumption that the hormone effect was mediated by cyclic AMP was supported by the findings that the cellular levels of cyclic AMP were elevated in the presence of glucagon and that dibutyryl cyclic AMP could replace glucagon as an effective inhibitor. The conclusion that the hormone effect was on uptake rather than on subsequent regurgitation was based on the linearity of accumulation in both the presence and absence of glucagon and the inability of glucagon to stimulate loss of invertase from preloaded cells. Colchicine and vinblastine also inhibited uptake. This finding and those of others which are discussed suggest the possibility that effects of cyclic nucleotides on certain cell functions may involve their regulation of microtubular status.
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PMID:Effect of glucagon on pinocytosis by the yolk sac of the rat. 90 54

Rat small bowel was perfused in vivo and ex vivo in the absence of biliary and pancreatic secretion. Intraluminal release of sucrase, alkaline phosphatase, aminopeptidase and enterokinase was significantly increased after administration of PG E1 and E2 1 and 5 microgram/kg. This suggests a direct stimulation of the intestinal mucosa, which might be mediated through cyclic AMP; dibutyryl cAMP significantly stimulates intraluminal release of proteins, sucrase and enterokinase.
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PMID:Prostaglandins E1 and E2 stimulate release of intestinal brush border enzymes. 90 72

The mechanism of hydroxy fatty acid-induced secretion was investigated in perfused hamster small intestine in vivo. Sodium ricinoleate at an 8-mM concentration resulted in not only secretion of water and sodium, but an increase in intestinal clearance of inulin and a 16,000 mol wt dextran as well. A concentration of ricinoleate (2 mM) which did not affect water transport, however, did not alter intestinal permeability. Ricinoleate-induced intestinal secretion was also accompanied by increased mucosal cell exfoliation as measured by the appearance of DNA in the perfusate and by apparent injury to epithelial cell membranes as judged by measurement of sucrase activity and phospholipid in cell-free aliquots of luminal fluid. Light and electron microscopic studies demonstrated substantial mucosal architectural changes with 8 mM ricinoleate with villus shortening and injury to epithelial cells at the villus tips. In contrast, cholera enterotoxin caused marked secretion of sodium and water, presumably by a cyclic AMP mechanism, but did not alter inulin clearance or enhance DNA or sucrase appearance in the lumen. These studies suggest that at least a component of ricinoleate-induced intestinal secretion is related to structural alterations of the mucosa.
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PMID:The effects of sodium ricinoleate on small intestinal function and structure. 95 72

The acute effects of intraduodenal administration of ethanol, 5 g/kg body weight, on intestinal activities of lipid-reesterifying and disaccharidase enzymes of the small bowel were studied. Results were compared to those produced in controls receiving isocaloric amounts of glucose by the same route. Acyl-CoA:monoglyceride acyltransferase, acyl-CoA synthetase (acid:CoA ligase (AMP) EC 6.2.1.3), sucrase, and lactase assays were performed on jejunal samples; acyl-CoA synthetase assay was performed on ileal samples. Ethanol produced greater activities of the lipid-reesterifying enzymes in the jejunum than did glucose. Ileal specific activity of acyl-CoA synthetase was also increased in the experimental group. No effect of ethanol on jejunal disaccharidase enzyme activities was noted. It is concluded that ethanol given acutely has a specific stimulating effect on intestinal enzymes involved in lipid absorption.
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PMID:The effect of acute ethanol treatment on lipid-reesterifying enzymes of the rat small bowel. 116 87

Nucleic acid synthesis in tissues of rapid growth is preferentially done using dietary purines and pyrimidines via the salvage pathway. In the case of a low protein intake, dietary nucleotides may be semiessential for cell replication of gut, lymphocytes, and bone marrow, and especially in those intestinal diseases in which the mucosa is altered, dietary nucleotides may have a role in intestinal development. The effect of dietary nucleotides on intestinal weight and length, gut mucosal weight, intestinal protein and DNA contents, and lactase, maltase, and intestinal mucosal activities was assessed in a controlled way. Weanling (21-day-old) rats were separated into two groups of 36, each receiving blindly a basal diet containing glucose polymers (C) or a basal diet with lactose as the main carbohydrate (L) for 15 days. Those fed with L developed a syndrome of chronic diarrhea and malnutrition. Ten rats of each group were sacrificed at that time. The rest of the animals of each group were separated into two subgroups. The first was fed with the C diet and the second with the C diet supplemented with 50 mg/100 g of each of the following nucleotides: AMP, GMP, CMP, UMP, and IMP (CN). Thus the subgroups CC, CN, LC, and LN were formed. Rats were sacrificed after 4 weeks and gut separated into three segments corresponding to duodenum, jejunum, and ileum. Analysis of variance was used to compare the effect of diet or segments. DNA and lactase, maltase, and sucrase activities increased in the LN group with respect to LC especially in jejunum and ileum but there were not any differences between CC and CN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary nucleotides on intestinal repair in rats with experimental chronic diarrhea. 212 43

The effects of somatostatin on cholera toxin-induced secretory diarrhea and the appearance of glycoenzymes in the intestinal lumen and intestinal lymph were investigated in rat small intestine. After exposure to cholera toxin, marked fluid accumulation in the small intestinal tract and elevation of the jejunal mucosal cyclic AMP (cAMP) concentration were observed. The activity of alkaline phosphatase, aminopeptidase and sucrase increased in the intestinal lumen after toxin exposure. In intestinal lymph, alkaline phosphatase activity was increased after cholera toxin administration, while aminopeptidase activity remained unchanged. Somatostatin suppressed cholera toxin-induced secretory diarrhea, but it did not affect the elevated mucosal cAMP concentration. This peptide also inhibited the appearance of glycoenzymes in the intestinal lumen and lymph induced by cholera toxin administration. These results suggest that somatostatin exerts its inhibitory effects on cholera toxin-induced secretory diarrhea and on the appearance of glycoenzymes in the intestinal lumen and lymph by affecting processes beyond cAMP formation.
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PMID:Inhibitory effect of somatostatin on cholera toxin-induced diarrhea and glycoenzyme secretion in rat intestine. 288 40

A halotolerant collagenolytic Vibrio alginolyticus strain isolated from salted hides had intracellular sucrase activity and did not secret sucrase into the medium. The strain actively transported sucrose by a sucrose-inducible, Na+-independent process. A 10.4-kilobase DNA fragment of V. alginolyticus DNA was cloned into Escherichia coli. The recombinant E. coli(pVS100) could utilize sucrose as a sole carbon source. In contrast to V. alginolyticus, the recombinant E. coli produced both intra- and extracellular sucrase activities. Up to 20% of the total sucrase activity was in the supernatant. Sucrase synthesis in E. coli(pVS100) was inducible and was subject to glucose repression, which was relieved by cyclic AMP. Sucrose was actively transported by a sucrose-inducible, Na+-independent system in E. coli(pVS100). Sucrose uptake was inhibited by the addition of a proton conductor. The maximum velocity and apparent Km values of sucrose uptake for the V. alginolyticus strain and E. coli(pVS100) were 130 nmol/mg of protein per min and 50 microM and 6 nmol/mg of protein per min and 275 microM, respectively.
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PMID:Expression and regulation of a Vibrio alginolyticus sucrose utilization system cloned in Escherichia coli. 303 63


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