Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.20 (alpha-glucosidase)
4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of Embelin, an experimental antifertility agent, to male rats (20 mg/kg body wt/day, daily for 15 and 30 days), caused an elevation in the uptake of D-glucose, L-alanine, L-leucine, and calcium in the small intestinal segments. An increase was also noted in the intestinal brush border membrane (BBM)-associated enzymes, sucrase, lactase, maltase, alkaline phosphatase, and leucine aminopeptidase in both the intestinal homogenates and partially purified BBM preparations, particularly after 30-day administration of the drug. Embelin treatment also caused a significant increase in the microsomal glucose-6-phosphatase and the cytosolic enzyme, lactate dehydrogenase. In the Embelin-treated animals BBM-associated total lipids, phospholipids, cholesterol, triacylglycerol, unesterified fatty acids, ganglioside-sialic acids as well as the cholesterol/phospholipids molar ratio showed a considerable increase. All these changes in the Embelin-treated animals were restored back to the normal or near normal biochemical makeup when the drug therapy was withdrawn and the animals were allowed to recover for another 15 and 30 days, respectively.
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PMID:Changes in glucose/amino acid/calcium uptake and brush-border membrane-associated enzymes in rat small intestine after the administration of embelin (plant benzoquinone), an antifertility agent. 211 47

The regulatory effect of epidermal growth factor (EGF) on the developmental pattern of brush border hydrolases was studied in the proximal jejunum and colon of the newborn rat. In the proximal colon, daily administration of EGF for 1, 3, or 5 days postpartum inhibited the postnatal increase in lactase, maltase, and aminopeptidase specific activities. In contrast, in the jejunum EGF did not influence lactase activity, inconsistently increased maltase activity, and partly prevented the early postnatal decrease in aminopeptidase activity. In the proximal colon, EGF showed additive effects with T4 and hydrocortisone on the inhibition of lactase activity. In the jejunum, EGF potentiated the effect of hydrocortisone and T4 on the expression of sucrase activity and had only a slight effect when injected alone. The incorporation rate of [3H]thymidine in the proximal colon and jejunum was not different in control and treated rats, indicating the absence of an effect of EGF on DNA synthesis. These results show that EGF may play an important physiological role in the enzymatic differentiation of the developing intestine during early postnatal development. Alone or acting with T4 or glucocorticoids, EGF may induce the decline of digestive hydrolases in the proximal colon. In the small intestine EGF may play a major role in the triggering of sucrase expression.
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PMID:Effect of epidermal growth factor on the expression of digestive hydrolases in the jejunum and colon of newborn rats. 211 92

We have described the methods used for studying the biosynthesis and the post-translational processing of sucrase-isomaltase (SI), lactase-phlorizin hydrolase (LPH) and maltase-glucoamylase (MGA) in human small intestinal mucosa. Our results are discussed in the context of findings by other researchers. A surprising finding coming out of all these studies is that SI, LPH and MGA are structurally quite different. SI and LPH are both synthesized as large molecular weight precursors which are proteolytically processed to the mature enzymes. In the case of SI, this processing occurs after insertion of the precursor into the brush border membrane and is catalysed by pancreatic proteases; the mature form consists of the two subunits sucrase and isomaltase, the latter containing an N-terminal peptide anchor. Proteolytic processing of the LPH-precursor occurs intracellularly, yielding a mature enzyme in the form of a two active site polypeptide which is anchored via a C-terminal peptide. The role of the large cleaved propolypeptide of LPH is not yet known. MGA is the largest of the three disaccharidases, having a molecular weight of greater than 300 kDa. No proteolytic processing seems to be taking place during biogenesis of MGA in human mucosa, and the mode of attachment to the membrane is unknown at present. The application of the methods described to the investigation of congenital sucrase-isomaltase deficiency (CSID) and lactase restriction in adults is presented and differences between CSID and LPH restriction are discussed.
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PMID:Molecular aspects of disaccharidase deficiencies. 211 33

A histochemical study of the time course of the appearance and location of lactase and alpha-glucosidase (used to detect sucrase and maltase) activities was carried out on control and rotavirus-infected mice from 7 to 14 days old. The overall pattern of enzyme activity was in agreement with previous quantitative studies on the activities of these enzymes. No evidence was obtained to support the idea that lactase deficiency was the result of repopulation of villi (denuded of lactase-producing villus cells) with immature lactase-negative cells. Low lactase activity was more likely to reflect profound changes in metabolically crippled cells, and recovery of lactase activity with recovery of normal metabolic functions. The location of enzyme activity to brush border regions rather than the cytoplasm of villus enterocytes enhances the significance of previous quantitative studies on these enzymes. The timing and duration of diminished lactase activities were such that they were unlikely to cause the induction or perpetuation of diarrhea in murine rotavirus diarrhea. The appearance in infected animals of alpha-glucosidase 3 days earlier than normal indicates that, in addition to reversible changes seen with lactase, developmental changes were accelerated that affected both crypt and villus cells.
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PMID:Disaccharidase activities in small intestine of rotavirus-infected suckling mice: a histochemical study. 212 44

Phase partitioning analyses of a brush border membrane preparation obtained with a divalent cation precipitation procedure (Am J Physiol 246:F853-F858, 1984) confirmed that Na+/H+ antiport activity was localized primarily to the brush border membrane of the rabbit proximal tubular epithelial cell. This analysis also indicated that antiport activity was associated with membrane populations that appeared to be derived from cytoplasmic structures. However, since the starting point of the analysis was a partially-purified brush border sample rather than a total membrane sample, it was not possible to discern the magnitude of the potential cytoplasmic pool of antiport activity. We have now used a three dimensional analytical fractionation procedure, based on differential centrifugation, equilibrium density gradient centrifugation, and partitioning in an aqueous polymer 2-phase system, to survey the subcellular distribution of Na/H antiport activity in rat kidney cortex. Roughly 53% of the recovered antiport activity could be assigned to a population of brush border membrane vesicles characterized by a 15-fold enrichment of maltase. An additional 26% of the recovered activity could be assigned to a group of three membrane populations whose biochemical characteristics appeared equally consistent with origins in distinct microdomains of the brush border membrane and with origins in microdomains of the Golgi complex involved in the assembly or recycling of brush border membrane constituents. Therefore, depending on the identities of membranes which contained the secondary pool of Na+/H+ antiport activity, no more than one-third of the total recoverable Na+/H+ antiport activity could be assigned to cytoplasmic membranes of the proximal tubular epithelium.
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PMID:Subcellular distribution of Na+/H+ antiport activity in rat renal cortex. 215 41

The antiulcerogenic drug ranitidine, given orally to mice, brought about reductions of kidney-bound hydrolytic enzymes at three different dose levels, viz. 10 mg, 100 mg, and 1000 mg/kg body weight, and for three different time points (single administration for 2 h and 24 h, and daily administration for 15 days). The activities of Na+, K(+)-ATPase, Ca2(+)-ATPase, and Mg2(+)-ATPase (marker enzymes of basolateral membranes) were reduced, and these reductions were significant at higher doses and after a 24-h single treatment or 15 days' daily treatment. Maltase, alkaline phosphatase, and leucine aminopeptidase (marker enzymes of brush border membrane [BBM]) activities were significantly inhibited after ranitidine treatment. Kinetic analysis of BBM-associated enzymes indicated that ranitidine decreased the maximum of apparent initial enzyme velocity (Vmax) of maltase, alkaline phosphatase, and leucine aminopeptidase. The substrate affinity constant (Km) was decreased in the case of alkaline phosphatase and maltase, while it was not altered in the case of leucine aminopeptidase. In vitro addition of ranitidine to renal BBM also produced significant inhibition of these enzymes, the inhibition constants (Ki) for maltase, alkaline phosphatase, and leucine aminopeptidase being 7.5, 15.5, and 3.5 mM, respectively. Membrane-bound lipid estimation showed a significant increase in phospholipids, triglycerides, and free fatty acids. Cholesterol, however, was decreased in both renal basolateral and brush border membranes.
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PMID:Effect of histamine H2-receptor antagonist, ranitidine on renal brush border and basolateral membranes. 217 15

To further document the effect of insulin on intestinal maturation, suckling rats were treated either with exogenous insulin (12.5 mU.g body wt, intraperitoneally, twice daily) or with saline from d 8 to 12 postpartum. Sucrase activity in brush border membrane extracts was precociously induced by insulin, whereas the activities of other brush border membrane enzymes (maltase, aminopeptidase, and neutral lactase) were enhanced (+ 30 to + 131%, p less than 0.01 versus controls). The lysosomal enzyme, N-acetyl-beta-glucosaminidase, which normally declines at weaning was significantly (p less than 0.025) decreased in both villus (-51%) and crypt cells (-57%) isolated from the jejunum of insulin-treated rats. The microsomal enzyme, sulfatase C, and the cytosolic enzyme, lactate dehydrogenase, were also sensitive to insulin with decreases in activity ranging from -37 to -63% (p less than 0.05) compared to saline-treated control rats. Insulin at doses of 0.5 or 12.5 mU did not influence plasma total corticosterone levels, which were about 9-fold lower in suckling than in 25-d-old weaned rats. In weaned rats (from d 25 to 32) insulin treatment (12.5 mU) failed to influence the activity of brush border membrane hydrolases or of lysosomal, microsomal, and cytosolic enzymes. The synthesis rate of mature sucrase-isomaltase, measured in weaned rats (32 d) by the incorporation of 14C-leucine into the enzyme precursor protein, was equivalent in both groups. These data demonstrate that the immature enterocyte of the suckling rat is responsive to insulin, whereas the mature enterocyte of the weaned rat is unresponsive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal regulation of the rat small intestine: responsiveness of villus and crypt cells to insulin during the suckling period and unresponsiveness after weaning. 217 34

The mechanisms by which the duodenal mucosa absorbs iron are unknown. Insorption into absorptive cells of luminal iron bound to transferrin via receptor-mediated endocytosis has been hypothesized, but transferrin and transferrin receptor are absent in apical microvillous brush borders of small bowel biopsies taken from fasted patients and normal volunteers. We hypothesized that a normal iron-containing diet might induce the transient appearance of transferrin and transferrin receptor in apical brush borders of small intestinal absorptive cells in a normal mouse that was provided iron-containing chow until the moment of sacrifice. Light and electron microscopic immunolocalization of transferrin and transferrin receptor in proximal small intestinal absorptive cells was limited to basolateral membranes and coated pits of cells predominantly in the crypts and basal regions of the villi. Transferrin and transferrin receptor were not detected in apical microvillous brush border membranes of these enterocytes. In parallel immunolocalization protocols designed to show the ability to immunodetect other antigens at these locations, maltase and proteoglycan were demonstrated in apical microvillous brush border membranes and in basolateral membranes, respectively, in absorptive cells of small intestinal villous tip, base, and crypt regions. Furthermore, transferrin and transferrin receptor were immunolocalized in hepatocyte sinusoidal microvillus membranes. We conclude that food does not induce the appearance of immunodetectable transferrin and transferrin receptor in the apical microvilli of small intestinal absorptive cells and, therefore, that these iron transport proteins are not involved in the apical microvillous membrane transport of luminal dietary iron.
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PMID:Immunolocalization of transferrin and transferrin receptor in mouse small intestinal absorptive cells. 218 90

The aim of this study was to assess the effects of Giardia muris on host growth and food intake, small intestinal morphometrics, mucosal enzyme activities, and brush border ultrastructure. Weanling mice infected with 1,000 G. muris cysts were compared to control and pair-fed sham-treated animals. Infection with G. muris resulted in decreased food intake and retarded growth. In infected animals, villus atrophy was observed in the duodenum throughout the study period and in the jejunum on days 8 and 50. On day 30, whereas jejunal architecture returned to normal in infected animals, malnourished pair-fed animals exhibited a compensatory increase in villus height. Sucrase and maltase were depressed in infected animals on days 2-24. On day 8 jejunal disaccharidases in pair-fed animals were also decreased but to a lesser extent than in infected animals. On day 24, disaccharidase values for control and infected mice were similar, whereas values in pair-fed animals were increased. On day 8, jejunal microvilli were shorter in infected animals than in control and pair-fed animals. This brush border injury was present throughout the jejunum and was also observed in pair-fed animals, but to a lesser extent. These findings suggest that G. muris retards growth in weanling mice, results in small intestinal injury, and interferes with the compensatory response to malnutrition of the infected host. Villus atrophy and brush border enzyme deficiencies associated with the disease mainly occur in the duodenum and jejunum, where trophozoites are most numerous. In infected and in pair-fed animals, the decrease in jejunal disaccharidase activities correlated with a diffuse shortening of brush border microvilli.
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PMID:Effects of murine giardiasis on growth, intestinal morphology , and disaccharidase activity. 219 Nov 3

The influence of epidermal growth factor (EGF) and hydrocortisone on the functional development of human fetal colon was studied in organ cultures. Fetal colon (14 to 17 weeks gestation) was cultured for 5 days at 37 degrees C in serum-free Leibovitz L-15 medium alone or supplemented with 1, 10, and 100 ng of EGF/ml or with 50 ng of hydrocortisone/ml of culture medium. The overall morphology of the colonic explants was not altered by the hormonal addition. In the continuous presence of EGF (1, 10, and 100 ng/ml) for 5 days, a significant decrease of [3H]thymidine incorporation into DNA was observed. At the brush border level, the addition of EGF induced a significant drop in sucrase, maltase, and alkaline phosphatase activities. These enzymic modifications occurred between the third and fifth day of culture, whereas variation in DNA synthesis was already evident within 24 h. The addition of hydrocortisone at a dose affecting the small intestine (50 ng/ml) did not significantly influence colonic DNA synthesis nor the digestive enzymic activities. These observations show for the first time that EGF, but not hydrocortisone, influences the proliferation and differentiation of human fetal colonic mucosa.
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PMID:Differential effects of epidermal growth factor and hydrocortisone in human fetal colon. 232 74


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