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

---

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

The alpha-glucosidase inhibitor acarbose induces a reversible delay of carbohydrate digestion. This action represents a new therapeutic option for the treatment of diabetes mellitus. The current investigation is a prospective, randomized double-blind crossover trial in 24 non-insulin dependent diabetics, fairly well controlled on diet alone or diet plus sulphonylurea. In periods of 10 weeks, the patients received successive treatment with acarbose and placebo in random order. A significantly lower HbA1 level and urinary glucose excretion were shown during acarbose as compared to placebo. The other parameters of diabetic control remained unchanged. Acarbose induced no significant alterations in the concentrations of important electrolytes, iron, vitamin B12 and folic acid. Although no major side effects occurred, meteorism and flatulence were frequent complaints. These data suggest that acarbose, in a dosage of 3 x 100 mg/day, is a safe drug, with slight beneficial effect on diabetic metabolic control.
...
PMID:Effects of acarbose on carbohydrate metabolism, electrolytes, minerals and vitamins in fairly well-controlled non-insulin-dependent diabetes mellitus. 177 45

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.
...
PMID:Immunolocalization of transferrin and transferrin receptor in mouse small intestinal absorptive cells. 218 90

We studied the activity and kinetic parameters of microvillous enzymes in intestinal villous cells and the concentration of the secretory component (SC) of p-immunoglobulin A in subcellular fractions of crypt cells in 35-day-old rats made iron deficient from birth and in controls. The aim of the study is to investigate the biochemical basis for the decreased activity of brush-border disaccharidases observed in growing animals with chronic iron deficiency. In rats made iron deficient, the specific (per unit protein) and the total (per total intestinal length) activities of sucrase, lactase, maltase, aminopeptidase, and diamine oxidase were decreased from -17 to -66% compared with the activities measured in the controls. The lower activity of sucrase in the brush-border membrane of the iron-deficient rats was associated with much slower enzyme synthesis rate than in control animals. Km of sucrase was identical in both iron-deficient rats and controls, but the maximum velocity of enzyme reaction was reduced proportionally to the enzymatic activity, indicating a lesser amount of enzyme rather than an inactivation. Electron microscopy of epithelial villous cells from iron-deficient rats revealed a marked rarefaction of secretory granules (transport vesicles) without apparent change in the morphology of the brush-border membrane or of cellular organelles. In villus and crypt cells isolated from the jejunum of iron-deficient rats, SC concentration was reduced to a level about half that of the controls. When SC concentration was measured in subcellular fractions of crypt cells, SC content in each fraction was two to three times lower in iron-deprived rats than in controls without evidence of accumulation of the protein at a given subcellular level.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Alteration of intracellular synthesis of surface membrane glycoproteins in small intestine of iron-deficient rats. 378 40

The weanling process is characterized by the transition from a liquid diet poor in iron (rat milk) to a solid diet high in iron (chow pellets). To examine the effects of iron content of the weanling diet on terminal maturation of rat small intestine, suckling pups, nursed by iron-sufficient mothers, were weaned by day 16 onto a solid basal diet that was either deficient [low-iron diet (LID): 0.5 mg iron/100 g solid] or high [high-iron diet (HID) controls: 30 mg iron/100 g solid] in iron. The animals were studied during or at the end of the 4th postnatal wk. By day 17 rats weaned onto the LID exhibited an initial rise in jejunal sucrase activity as did their controls, but the activity plateau of the enzyme was reduced to a level 60% of the controls. On day 28 iron-deprived rats were anemic and showed significant decreases (P less than 0.01 compared with HID rats) in the activity of jejunal sucrase (-57%), neutral lactase (-83%), and maltase (-46%), whereas villus height, crypt depth, mucosal mass parameters, ileal acid beta-galactosidase activity, mucosal protein, and DNA synthesis rates were equivalent in LID and HID groups. The concentration of the secretory component, a glycoprotein synthesized by the intestinal crypt cell, was markedly depressed (P less than 0.01 vs. controls) in the jejunum (-54%) and ileum (-79%) of iron-deprived rats. When D-[1-14C]glucosamine was injected intraperitoneally, incorporation of the label into jejunal and ileal brush-border proteins was two to three times lower for iron-deficient rats than for controls.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Role of dietary iron in maturation of rat small intestine at weaning. 674 22

Newborn rats born to iron deficient mothers (IDM) were found to have significantly lower hemoglobin, sucrase, lactase and maltase levels compared to control newborn rats. Rats born to IDM and nursed by IDM, when sacrificed at 21 days of age, had statistically significantly lower hemoglobin, serum iron, sucrase, lactase and maltase levels compared to control rats. Rats born to IDM, but nursed by iron sufficient mothers (ISM) and sacrificed at 21 days of age, had hemoglobin, serum iron and sucrase levels compared to control rats whereas lactase and maltase were not corrected by 21 days of nursing by ISM. Rats burn to IDM and nursed by either IDM or ISM for 21 days were given intramuscular iron dextran and placed on iron sufficient diet (ISD) for 7 days. These animals experienced correction of the hemoglobin, serum iron, sucrase and maltase levels compared to control rats, whereas intestinal lactase was not corrected by 7 days of ISD and intramuscular iron. Rats born to ISM, nursed by IDM and sacrificed on day 21 had significantly lower hemoglobin, serum iron and intestinal lactase levels compared to control rats. Rats both to ISM and nursed by IDM were given intramuscular iron dextran on day 21 and placed on an ISD from day 21-28. These animals had a return in hemoglobin, serum iron, sucrase and maltase levels comparable to control rats. Rats born to and nursed by ISM and maintained on an iron deficient diet from day 21-84 had significantly lower hemoglobin, serum iron, sucrase, lactase and maltase levels compared to control rats. Rats born to and nursed by ISM, maintained on iron deficient diet from day 21-84, and then given intramuscular iron dextran on day 84 and maintained on an ISD until day 92, experienced correction of the hemoglobin, serum iron and lactase levels compared to control rats. Intramuscular iron and 7 days of ISD did not correct the sucrase and maltase levels in these rats. Lactose tolerance tests in iron deficient rats showed flat curves compared to controls. After iron treatment, lactose tolerance curves returned to control values. Iron deficiency in rats in utero, during the nursing and postweaning period causes, in addition to anemia, a reduction in jejunal disaccharidase activity because of an alteration in the enzymes of the brush border membrane. Varying degrees of reduction and response of certain disaccharidases to iron treatment are dependent on the time of iron deprivation in relationship to the intra-uterine and postnatal development of the digestive and absorptive functions in the small intestine. Alterations in the levels of disaccharidases demonstrated in this paper represents another aspect of the spectrum of biochemical effects of iron deficiency.
...
PMID:Disaccharidase levels in iron deficient rats at birth and during the nursing and postweaning periods: response to iron treatment. 707 2

Neutral alpha-glucosidase levels as epididymal marker, fructose levels as vesicular marker, zinc, citric acid and prostate specific antigen levels as prostatic markers were measured in the seminal plasma of eight transfusion-dependent beta-thalassemic patients in order to study epididymal and sex accessory gland secretions (eighteen subjects served as controls). FSH and LH as well as total and free testosterone were detected displaying unaltered serum values. Ejaculate of patients showed normal sperm count and low sperm motility, in the meantime seminal plasma exhibited unaltered both neutral alpha-glucosidase and fructose values but low levels of zinc, citric acid and prostate specific antigen were noticed as well. These data suggest an impaired prostatic secretion in the thalassemic patients studied. A local iron toxicity on the prostatic tissue could be supported by the decrease of its specific markers observed only in the subgroup of patients with high ferritin serum levels.
...
PMID:Epididymal and sex accessory gland secretions in transfusion-dependent beta-thalassemic patients: evidence of an impaired prostatic function. 922 14

Iron-deficiency anemia is the nutritional deficiency most frequently occurring throughout the world, which manifests as a complex systemic disease involving all cells, affecting enzyme activities and modifying protein synthesis. In view of these considerations, the objective of the present study was to determine the effects of iron-deficiency anemia on disaccharidases and on the epithelial morphokinetics of the jejunal mucosa. Newly weaned male Wistar rats were divided into 4 groups of 10 animals each: C6w received a standard ration containing 36 mg elemental iron per kg ration for 6 weeks; E6w received an iron-poor ration (5-8 mg/kg ration) for 6 weeks; C10w received an iron-rich ration (36 mg/kg ration) for 10 weeks; E10w received an iron-poor ration for 6 weeks and then an iron-rich ration (36 mg/kg) for an additional 4 weeks. Jejunal fragments were used to measure disaccharidase content and to study cell proliferation. The following results were obtained: 1) a significant reduction (P < 0.001) of animal weight, hemoglobin (Hb), serum iron and total iron-binding capacity (TIBC) in group E6w as compared to C6w; reversal of the alterations in Hb, serum iron and TIBC with iron repletion (E10w = C10w); animal weights continued to be significantly different in groups E10w and C10w. 2) Sucrase and maltase levels were unchanged; total and specific lactase levels were significantly lower in group E6w and this reduction was reversed by iron repletion (E10w = C10w). 3) The cell proliferation parameters did not differ between groups. On the basis of these results, we conclude that lactase production was influenced by iron deficiency and that this fact was not related to changes in cell population and proliferation in the intestinal mucosa.
...
PMID:Disaccharidase levels in normal epithelium of the small intestine of rats with iron-deficiency anemia. 936 8

Excessive chronic ethanol administration to animals has been shown to cause oxidative insults to many body organs, including the liver and brain. In many instances, iron supplementation to the diet may further aggravate ethanol-induced liver damage. However, whether increased dietary iron can enhance the damage in the brain is unknown. In this study, four groups of Sprague-Dawley rats were fed a Lieber-DeCarli liquid diet containing 5% (w/v) ethanol or isocaloric amount of maltase and/or 0.25% (w/v) carbonyl iron for 2 months. At the end of the feeding regimen, iron contents were determined in the plasma, liver, cerebral cortex, and cerebellum. Cerebellar superoxide dismutase (SOD) and nitric oxide synthase (NOS) activities were measured and mRNA levels of MnSOD, CuZnSOD, and nNOS in the cerebellar granule cell layer were quantitated by in situ hybridization. Ethanol treatment alone caused an increase in iron levels in plasma, no change in the liver and cerebral cortex, but a decrease in the cerebellum. Iron supplementation increased liver iron >4-fold but did not alter iron contents in the cerebellum and cortex. All of the mRNA species examined and SOD activity were not affected by either iron or ethanol administration. However, NOS activity in the cerebellum was significantly enhanced by ethanol, whereas iron supplementation had an opposite effect. Our results indicate that iron supplementation to animals consuming ethanol may have tissue-specific effects. Furthermore, ethanol-induced increase in NOS activity in the cerebellum may explain the sensitivity of cerebellar neurons to oxidative insult.
...
PMID:Chronic ethanol and iron administration on iron content, neuronal nitric oxide synthase, and superoxide dismutase in rat cerebellum. 1023 6

Hypolactasia associated with severe iron-deficiency anemia has been reported in several studies. The objective of the present study was to determine whether hypolactasia is associated with the degree and duration of iron-deficiency anemia. Newly weaned male Wistar rats were divided into a control group receiving a diet supplemented with iron (C) and an experimental group (E) receiving a diet not supplemented with iron (iron-deficiency diet). The animals were studied on the 3rd, 5th, 7th, 14th, 21st, 28th and 35th days of the experiment, when overall and iron nutritional status and disaccharidase activity in the small intestine were determined by the Dahlqvist method. A reduction in weight occurred in the anemic animals starting on the 5th day of the study. Anemia was present in the experimental animals, with a progressive worsening up to the 14th day (hemoglobin: C = 13.27 and E = 5.37) and stabilizing thereafter. Saccharase and maltase activities did not differ significantly between groups, whereas lactase showed a significant reduction in total (TA) and specific activity (SA) in the anemic animals starting on the 21st day of the study. Median lactase TA for the C and E groups was 2.27 and 1.25 U on the 21st day, 2.87 and 1. 88 U on the 28th day, and 4.20 and 1.59 U on the 35th day, respectively. Median lactase SA was 0.31 and 0.20 U/g wet weight on the 21st day, 0.39 and 0.24 U/g wet weight on the 28th day, and 0.42 and 0.23 U/g wet weight on the 35th day, respectively. These findings suggest a relationship between the enzymatic alterations observed and both the degree and duration of the anemic process. Analysis of other studies on intestinal disaccharidases in anemia suggests that the mechanism of these changes may be functional, i.e., that the enterocytes may suffer a reduction in their ability to synthesize these enzymes.
...
PMID:Relation of the disaccharidases in the small intestine of the rat to the degree of experimentally induced iron-deficiency anemia. 1077 85

Ferroplasma acidiphilum strain Y (DSM 12658), a ferrous iron-oxidizing, acidophilic and mesophilic archaeon, was found to produce a membrane-bound alpha-glucosidase (alphaGluFa) showing no significant similarity to any of the known glycoside hydrolases classified in different families and having an unusual catalytic site consisting of a threonine and a histidine residue. The highest alpha-glucosidase activity was found at low pH, 2.4-3.5, and the substrate preference order was: sucrose>maltose>maltotriose >>maltotetraose>>malto-oligosaccharides from maltopentaose to maltoheptaose>>>soluble starch (kcat/K(m) was 293.0, 197.0, 18.8, 0.3 and 0.02 s(-1) x mM(-1) respectively). The enzyme was able to transfer glucosyl groups from maltose as donor, to produce exclusively maltotriose (up to 300 g/l). Chemical modification and electrospray ionization MS analysis of 5-fluoro-alpha-D-glucopyranosyl-enzyme derivatives, coupled with site-directed mutagenesis, strongly suggested that the putative catalytic nucleophile in this enzyme is Thr212. Iron was found to be essential for enzyme activity and integrity, and His390 was shown to be essential for iron binding. These results suggest that the metalloenzyme alphaGluFa is a new member of the glycosyl hydrolase family that uses a novel mechanism for sugar glycosylation and/or transglycosylation.
...
PMID:A novel alpha-glucosidase from the acidophilic archaeon Ferroplasma acidiphilum strain Y with high transglycosylation activity and an unusual catalytic nucleophile. 1595 64


1 2 Next >>

---