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)

Differential centrifugation of rat small intestinal homogenates produced a crude brush border (BB) fraction that was enriched 15-fold for the marker enzymes, alkaline phosphatase and sucrase; contamination with mitochondrial enzymes, monoamine oxidase and succinate dehydrogenase, was minimal. ATP hydrolysis by this BB fraction was stimulated by addition of several anions to the incubation medium: HCO3 and Cl were equally effective in this regard, with NO3, NO2, SO4, and acetate being less stimulatory. SCN and CNO inhibited ATPase activity, whereas the divalent anion SO3 was stimulatory at low concentrations (less than 25 mM) but inhibitory at 100 mM. Maximum anion stimulation was observed at a Mg concentration of 0.5 mM, and pH optimum was 8.5. Kinetic analysis showed that HCO3 increased the Vmax without altering the Km for ATP; the Ka for this effect of HCO3 was 35 mM. This enzyme activity was completely inhibited by 20 mM L-phenylalanine, 10 mM L-cysteine, and 3 mM EDTA, compounds that also inhibited intestinal alkaline phosphatase. These results demonstrate the presence of anion-stimulated ATPase activity in rat small intestinal brush border and suggest that this activity may be related to intestinal alkaline phosphatase. The role of this enzyme in intestinal transport is not known, but could relate to the regulation of intestinal absorption and secretion.
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PMID:Anion-stimulated ATPase activity of brush border from rat small intestine. 15 3

Thyroid hormone [triiodothyronine (T3)] has been shown to play a critical role in the growth and maturation of the mammalian small intestine, but its mechanism of action has not been well studied. In the current study, an animal model of hypothyroidism and hyperthyroidism was used to study the effects of T3 on the small intestine. Adult rats were treated with propylthiouracil for a 6-week period and then given injections of either saline (hypothyroid) or 30 micrograms/100 g body wt of T3 (hyperthyroid). Northern blot analyses showed marked differential regulation of brush border enzyme gene expression. Lactase messenger RNA (mRNA) levels decreased approximately 75% along the length of the small intestine, whereas sucrase levels were unchanged. The intestinal alkaline phosphatase mRNA species were upregulated by T3, especially the 3-kilobase band, which increased most dramatically in jejunum. Further experiments showed significant levels of both the alpha-1 and beta-1 T3 receptor mRNAs within the small intestinal mucosa. Histological examination showed that T3 treatment causes marked villus hyperplasia throughout the length of the small intestine. These results provide insight into the mechanism by which T3 exerts its influence on the growth and differentiation of the intestinal epithelium.
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PMID:Thyroid hormone differentially regulates rat intestinal brush border enzyme gene expression. 138 52

We have reported the appearance of surfactant-like particles enriched for intestinal alkaline phosphatase and phosphatidylcholine within enterocytes and in the lumen of adult fat-fed rat intestine. Because rat pulmonary surfactant decreases in abundance during the first postnatal days, we examined the developmental expression of these intestinal particles in suckling rats. Electron microscopy revealed abundant particles in 1-day-old rats within and surrounding the villus enterocytes, declining in frequency by day 14. Phosphatidylcholine content, alkaline phosphatase, sucrase-isomaltase, and lactase activity in particles peaked 1 day after birth, declining rapidly to adult levels by day 3 of life, except for sucrase, which peaked again after weaning. The postnatal developmental profile of the same brush-border-associated enzymes was totally different. Membrane fractions enriched for alkaline phosphatase and of similar density to rat surfactant-like particles were isolated from the small intestine of an amphibian (Xenopus laevis) and a fish (grass carp). Electron microscopy of the Xenopus membranes revealed unilamellar structures similar to the rat particles, but the carp membranes were of dissimilar morphology. We conclude that particles with surfactant-like properties in the rat intestine are ontogenically expressed like pulmonary surfactant; similar particles are evident only in animals with lungs.
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PMID:Developmental expression of intestinal surfactant-like particles in rats. 187 97

Intestinal Ca2+ malabsorption has been described in spontaneously hypertensive rats (SHRs), but the molecular basis for this defect is unknown. In this study, we measured intestinal alkaline phosphatase and vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins implicated in the active pathway of intestinal Ca2+ absorption. Both proteins were measured in the small intestines of SHRs and their normotensive controls, Wistar-Kyoto rats, before, during, and after development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages, alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57% (P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm) (P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The decreases of calbindin were statistically significant (P less than 0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than 0.001-0.005). Decreased calbindin in SHRs was documented in animals from two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase could not be attributed to malnutrition or to a generalized brush-border defect as indicated by body weights and the intestinal marker enzyme sucrase. Although calbindin-D9k was decreased in young SHRs, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in 4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum 1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats. 203 38

We report results on determinations of small intestinal brush-border enzyme activities in 22 children (aged 11 months to 14 years) with giardiasis. In particular, activities of disaccharidases (lactase, sucrase, maltase) and of alkaline phosphatase were investigated. Forty-one percent of the patients, irrespective of age, had a demonstrable depression of disaccharidase activities, usually in a combination involving two or more enzymes. A depression of intestinal alkaline phosphatase activity was present in 33% of patients, and only in those who demonstrated disaccharidase deficiencies. Mild villus atrophy was present in two mucosal specimens, whereas all others showed normal villus morphology by light microscopy. The results obtained in this study suggest that giardiasis in otherwise healthy children does not cause marked structural damage to the small bowel mucosa, as seen by the light microscope. However, some form of damage to the brush border does occur frequently, as evidenced by a depression of brush-border enzymes. This damage most likely contributes to the diarrhea and also to the carbohydrate intolerance in these patients.
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PMID:Intestinal disaccharidase and alkaline phosphatase activity in giardiasis. 642 May 34

In order to clarify the mechanism of the adverse effects of dietary amaranth, trisodium 1-(4-sulfo-1-naphthylazo)-2-naphthyl-3,6 disulfonic acid, the effects of amaranth in vitro and in a jejunum perfusion in vivo on intestinal sucrase were investigated in rats. The inhibitory effect of amaranth in vitro on the sucrase activity was not detected even at the concentration of 1%, whereas the remarkable release of intestinal sucrase from intestine was observed with the jejunum perfusion of Ringer bicarbonate solution (RBS) containing amaranth at the 1% level. On the other hand, the perfusion of RBS containing tris(hydroxymethyl)-aminomethane, a strong inhibitor of intestinal disaccharidase activities, did not produce the release of intestinal alkaline phosphatase. These findings suggest that the toxicity of dietary amaranth is due to the exfoliating or solubilizing effects of amaranth on the brush border membrane of the small intestine.
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PMID:Mechanisms of adverse effect of amaranth feeding in the rat. 688 37

The relation between food intake and enzyme activity of the small intestine and rate of intestinal absorption were studied in rats 15 days after induction of alloxan diabetes. Diabetic rats were given an ad lib. semisynthetic diet or a restricted diet on the basis of either daily intake or body weight. The rates of absorption of 5 mMD-galactose and L-valine were determined in vitro by the everted sac method. The rates of absorption of the substances, expressed per unit weight or per length of intestine, were higher in diabetic rats than in controls, regardless of the amount of food consumed. Maltase and sucrase activities were significantly increased in diabetic rats, regardless of the amount of food consumed. The activity of intestinal alkaline phosphatase was increased in diabetic rats fed ad lib., but not in those on a restricted diet. These findings suggest that in alloxan diabetic rats the increased disaccharidase activity in the small intestine is due to insulin deficiency, and that the increased activity of alkaline phosphatase is only a secondary effect of insulin deficiency, caused by increased food intake resulting from insulin deficiency.
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PMID:Effect of food intake on intestinal absorption and mucosal hydrolases in alloxan diabetic rats. 698 35

The present study was designed to investigate the effects of grape seed tannins on rat intestinal alkaline phosphatase (AP), sucrase and dipeptidyl peptidase IV (DPP IV) activities. An experiment was performed in vivo by dietary supplementation with 2% tannins; this diet was tested on an experimental group of rats; a control group received a diet without tannins. After 31 days, tannins intake significantly decreased middle-jejunal AP from 123 to 45 mU/mg protein and sucrase activities from 310 to 195 mU/mg protein, while no significant difference appeared at the duodenal stage (p < 0.05). Ileal DPP IV activity was also significantly reduced (p < 0.05) from 190 to 110 mU/mg protein after tannin intake. Using in vitro experiments on purified brush border membranes, AP activity was found to be inhibited by grape tannins; this inhibition was prevented by the detergent Triton X-100. The addition of pancreatic-biliary (PB) juice to the incubation medium prevented or reversed the tannin-inhibited enzyme activity. The present data indicate that in the duodenal lumen, alkalinity and detergency from the PB secretion neutralized the ability of tannins to inactivate brush border hydrolase activities and suggest that enzyme inhibition took place once bile salts were reabsorbed while moving down the gut. This was confirmed by in vitro experiments where sucrase and DPP IV activities inhibited by grape seed tannins were largely recovered after the addition of PB juice to the incubation medium.
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PMID:Effect of grape seed tannins on the activity of some rat intestinal enzyme activities. 778 71

The obese spontaneous hypertensive rat/NIH-corpulent (SHR/N-cp) rat exhibits some of the metabolic and pathologic alterations associated with non-insulin-dependent diabetes mellitus and hypertension. The current study was conducted to investigate the influence of phenotype (ob versus In) and source of dietary carbohydrate (sucrose versus starch) on intestinal sucrase, maltase, lactase, and alkaline phosphatase activity in SHR/N-cp rats. For 3 months, lean and obese male SHR/N-cp rats were fed isocaloric diets containing as the sole source of carbohydrate either 54% cooked corn starch or sucrose. Serum and urine markers for diabetes were observed in obese rats. Wet weight and length of intestines were significantly increased in obese rats compared with lean littermates. Among the intestinal enzymes measured, statistical tests confirmed that sucrase activity was significantly increased (P < 0.01) by both phenotype (ob > In) and feeding a sucrose diet. Diet alone (sucrose > starch) significantly increased (P < 0.05) maltase activity in obese rats, but had no effect on lean rats. Lactase activity was significantly higher (P < 0.05) in obese sucrose-fed rats compared with obese starch-fed and/or lean littermates. Statistical tests revealed that intestinal alkaline phosphatase activity was significantly altered (P < 0.05) by both phenotype and diet. Intestinal alkaline phosphatase was higher in starch-fed lean rats compared with lean littermates fed sucrose and to starch or sucrose-fed obese rats. These results are not indicative of a simple, nonspecific increase in intestinal enzyme activity, since the effects observed in intestinal alkaline phosphatase contrast the effects observed in intestinal sucrase, maltase, and lactase activity. These results indicate that both phenotype and diet alter structural and enzymatic intestinal activities of SHR/N-cp rats. Distinct variations in the observed intestinal enzymatic activities suggest that these enzymes are under the control of genetic, hormonal, and dietary factors. Rationale for these differences are discussed.
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PMID:Effect of dietary carbohydrate and phenotype on sucrase, maltase, lactase, and alkaline phosphatase specific activity in SHR/N-cp rat. 843 90

The molecular events that regulate differentiation of human colon mucosal cells are not known. Although a number of in vitro models to study this question exist, none have identified a gene product which could function as a mediator of cell differentiation. Although the Ki-ras gene is frequently mutated in human colon cancer, the Ha-ras protooncogene is maximally expressed in the most differentiated cells of intestinal mucosa. In order to study the effects of Ha-ras gene overexpression on the differentiation phenotype in human colon cancer cells, we have expressed the v-rasH oncogene in CaCO2 cells. This maneuver resulted in a marked induction of gene expression of multiple markers characteristic of intestinal brush border differentiation. These include a > or = 30-fold induction of sucrase, a 10-fold increase in intestinal alkaline phosphatase, a 20-fold induction of transforming growth factor alpha, and a 5-fold increase in transforming growth factor beta 1 steady-state mRNA levels. Finally, the CaCO2-ras cells undergo a > or = 95% reduction in DNA synthesis under serum-deficient conditions and cannot be restimulated after such treatment, suggesting terminal differentiation, whereas the same treatment has no effect on the proliferative capacity of the parent CaCO2 cell line. These studies with CaCO2 human colon cancer cells provide a model to study the role of v-rasH and related genes in colon epithelial differentiation.
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PMID:Induction of markers of normal differentiation in human colon carcinoma cells by the v-rasH oncogene. 849 94


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