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)

The effects of increasing environmental temperature and of exercise on some biochemical characteristics of the intestinal mucosa were analyzed in hamsters to determine whether damage occurs to the intestine during exercise, because long-distance runners complain of cramp, diarrhea, or retrostaltic symptoms, especially when exercise is performed at high temperatures. Two sets of experiments were carried out on groups of five animals. First, one group stayed at rest at 20 degrees C while another group performed exercise for 30 min at the same temperature. Second, one group of animals remained at rest at 20 degrees C for 16 h, a second group was placed at 32 degrees C for the same period, and a third group was subjected to the latter treatment but in addition performed two 20-min exercises. The animals were killed immediately after the experiment. After the small bowel was removed, biopsies were taken for histological examination, and the remaining small bowel tissue was homogenized for biochemical analysis. During exercise performed at 20 degrees C or during exposure to 32 degrees C, the DNA weight (expressed as a function of the protein weight) increased; the specific activity of sucrase, leucine aminopeptidase, diamine oxidase, and maltase decreased; spermine and putrescine content generally decreased; and the weight of mucosal proteins per length of intestine did not vary significantly. When exercise was performed at 32 degrees C, we noted few modifications in the values of the intestinal parameters tested, i.e., changes in only the weight of mucosa expressed as a function of bowel length and, perhaps, the spermine or putrescine content.
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PMID:Effects of environmental temperature and exercise on the biochemical characteristics of hamster intestine. 202 50

The protective effect of N-benzyl-D-glucamine dithiocarbamate (BGD) against gastrointestinal and bone marrow toxicities produced by cis-diamminedichloroplatinum (DDP) injection in rats was studied. Rats were injected i.p. with BGD (2 mmol/kg) immediately after i.v. injection of DDP (20 mumol/kg). A scanning electron micrograph of the jejunum after DDP treatment showed damage in the villi, and that BGD protected the DDP-induced jejunal damage. BGD treatment also had a protective effect against DDP-induced diarrhea. BGD significantly reversed the reduction in maltase and sucrase activities of jejunal mucosa of rats treated with DDP. Platinum (Pt) concentrations in the gastrointestine as well as in the kidney and liver after DDP injection decreased following BGD treatment. The reduction of leukocytes following DDP injection returned to control values after BGD treatment. Biliary and urinary excretions of Pt after DDP injection was remarkably increased by BGD treatment. The results of this study indicated that the injection of BGD to rats treated with DDP can effectively remove Pt from the body through biliary and urinary excretions, resulting in protection of the gastrointestinal and bone marrow toxicities induced by DDP treatment.
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PMID:Protective effect of N-benzyl-D-glucamine dithiocarbamate against cis-diamminedichloroplatinum-induced toxicity in gastrointestinal tract and bone marrow in rats. 208 97

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

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

This double-blind study was performed to evaluate the relation of the glycemic and hormonal (insulin, gastric inhibitory polypeptide) responses to standardized starch and sucrose meals to signs (H2 exhalation) and subjective symptoms of carbohydrate malabsorption during administration of 100 mg BAYm 1099 (miglitol) t.i.d. over a period of 8 weeks. Two groups of 8 male healthy volunteers received either placebo or verum. Oral sucrose loading tests (50 g) with and without miglitol were performed at day -5, 1, 25 and 53 of the study, starch loading tests (50 g) with and without the inhibitor were carried out at day -2, 4, 28 and 56. Miglitol significantly flattened the glycemic responses to sucrose and starch without evidence of diminished efficacy over the 8-week period. Also the blunting effect of miglitol on serum insulin and gastric inhibitory polypeptide responses and the stimulation of breath hydrogen exhalation proving carbohydrate malabsorption with starch and sucrose remained unchanged over time. Comparing breath hydrogen exhalation, responses were more pronounced after sucrose than after the starch loading tests. Symptoms (bloating, flatulence, diarrhea, cramps) were merely noticeable with starch as the substrate, but clearly present after sucrose. These symptoms were substantially curtailed during continuous drug intake. It is concluded that - irrespective of the substrate (starch/sucrose) - there is no escape of the desired effects of alpha-glucosidase inhibition by miglitol over 8 weeks, but symptoms of gaseousness due to carbohydrate malabsorption may undergo habituation.
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PMID:Postprandial glycemic control, hormonal effects and carbohydrate malabsorption during long-term administration of the alpha-glucosidase inhibitor miglitol. 229 49

Physicians studied 16 moderately to severely malnourished infants 6 months old who had severe diarrhea for 2 weeks and did not gain weight. After admitting the infants, they administered total parenteral nutrition (TPN) to the infants through a central vein. As the infants began receiving TPN, they were randomly assigned to receive either banked human milk or sterile water by continuous nasogastric feeding for 2 weeks. In addition, before beginning nasogastric feedings and at the conclusion of the study, a physician performed a peroral biopsy of the small intestine. Small intestine perfusion studies were also done in the beginning and at the end of the 2 week period. More infants in the human milk group than in the sterile water group had 25% decrease in sucrase activity (p.02). Researchers noted that the villus/crypt ratio was similar in both groups at the beginning of the study and improved only in the sterile water group (p.002), but this was not a function of treatment. Additionally, more infants in the human milk group had an increase in the intraepithelial lymphocyte count than those in the sterile water group (milk, 5/7; water, 1/8; p.03). On the other hand, the data demonstrate that no differences existed in glucose and water absorption or in lactase and maltase activities as a function of the milk versus water treatment. Therefore, the results of this study suggest that human milk does not benefit small intestine mucosa recovery. Research to determine the effect of predigested formulas or specific factors in fresh human milk on the rate of mucosal recovery is needed.
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PMID:Human milk and the rate of small intestinal mucosal recovery in protracted diarrhea. 249 97

To study the effects of acarbose, an alpha-glucosidase inhibitor, on saccharide absorption and pancreatic and gut hormone release, we loaded 50 g glucose (GTT), maltose (MTT), and sucrose (STT) to 12 healthy male volunteers with and without acarbose (0, 100, or 300 mg) in a double-blind protocol. Oral load of 300 mg acarbose did not inhibit absorption of 50 g glucose; neither did it alter subsequent responses of insulin and glucagons. Maltose absorption was not influenced by acarbose up to 300 mg. However, insulin response was reduced and eteroglucagon response was enhanced by acarbose. Acarbose 100 mg markedly decreased absorption of sucrose, resulting in inhibition of plasma elevation of glucose and insulin and in enhancement of enteroglucagon release. Oral load of 30 g lactulose, nonabsorbable disaccharide, could reproduce the acarbose-induced enteroglucagon release. An increase in osmotic pressure due to retention of unabsorbed carbohydrate in the distal small intestine and proximal colon may explain the acarbose-induced enteroglucagon release and diarrhea that results from STT with acarbose.
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PMID:Enteroglucagon release in disaccharide malabsorption induced by intestinal alpha-glucosidase inhibition. 265 36

To investigate further the pathophysiology of rotavirus-induced diarrhea, changes in specific activities of eight relevant intestinal enzymes [alkaline phosphatase, thymidine kinase, lactase, maltase, sucrase, Na+,K+-adenosine triphosphatase (ATPase), adenylate and guanylate cyclases] were measured following infection of suckling mice with murine rotavirus (epizootic diarrhea of infant mouse strain) and compared with age-matched control mice. The concentration of lactose within the lumen of the gastrointestinal tract during infection was also measured. During the course of infection, activities of alkaline phosphatase and lactase decreased, whilst the activity of thymidine kinase increased. Precocious maturation profiles of sucrase and maltase enzymes were observed. No significant changes were detected in the activities of Na+,K+-ATPase or the adenylate and guanylate cyclases. These results are discussed in relation to existing and novel hypotheses on the pathogenesis of rotavirus-induced diarrhea.
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PMID:Intestinal enzyme profiles in normal and rotavirus-infected mice. 289 74

Oral feeding of DL-difluoromethyl ornithine (DFMO) (2% in water ad libitum) for 14 days has no detectable effect on the small intestine of adult rats. Similar feeding of DFMO to weanling rat pups caused diarrhea in three to four days accompanied by a decrease in food consumption and body weight compared to age-matched controls. Significant decreases in small intestinal mucosal weight, total protein, DNA, enterokinase, leucine amino peptidase, sucrase, and maltase contents were observed in the DFMO-treated group four days after treatment. Extending the treatment to seven days led to a more severe reduction in these parameters. Villous atrophy of the mucosa was demonstrable by light microscopy and morphometric measurements. The mucosa of the DFMO-treated rat pups showed a reduction in total thickness and villous height but no change in crypt depth. A significant reduction in villus-crypt ratio was also seen. Changes in small intestinal mucosal parameters were not due to a decrease in food intake since pair-fed, age-matched rat pups showed no biochemical changes compared to control pups. DFMO-treated weanling rats showed less than 5% of ornithine decarboxylase (ODC) activity when compared to age-matched control animals. The effects observed on the small intestinal mucosa are presumably due to inhibition of ornithine decarboxylase activities by DFMO which prevents the proliferation, regeneration, and maturation of epithelial cells. The relative insensitivity of the adult rat small intestine to DFMO treatment suggests a lesser dependence of its intestinal mucosa to ODC activities.
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PMID:Effect of difluoromethyl ornithine (DFMO) on small intestine of adult and weanling rats. 311 4

1. Biochemical estimates of lactase, sucrase and maltase activities, carried out on intestinal biopsies appearing histologically normal, were compared with those obtained from children suffering from coeliac disease, cow's milk protein intolerance/postenteritis syndrome and the intractable diarrhoea syndrome of infancy. Lactase deficiency in these children was found to be more pronounced than sucrase or maltase deficiencies. 2. Quantitative cytochemical investigations showed characteristic disease-induced changes in the ability of enterocytes to express alpha- and beta-glucosidases, but not alkaline phosphatase activities, during migration along stunted villi. 3. Separate estimates of the time course describing hydrolase development in normal and coeliac tissue showed the initial rate of lactase appearance to be halved in coeliac patients, while that for alpha-glucosidases remained constant and that for alkaline phosphatase increased by a factor of four. Enteroblastic replacement of mature enterocytes cannot provide a general explanation for hydrolase deficiency in diseased intestine.
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PMID:Selective alteration of brush-border hydrolases in intestinal diseases in childhood. 312 20


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