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)

Thirty infants with intractable diarrhea of infancy (IDI) underwent small bowel biopsies in order to determine the extent and duration of small intestinal mucosal injury. The onset of the persistent diarrhea occurred prior to 3 months of age and continued for an average of 48 days prior to investigation. In 18 cases, no associated entities were found. Mucosal injury was invariably found in all 30 infants: grade IV injury in 11, grade III in eight, grade II in nine, and grade I atrophy in one. Disaccharidase activities were diminished and corresponded to the degree of atrophy. Lactase activity was diminished to a greater extent than sucrase and maltase. Significant, persistent mucosal injury existed for an average of six months in 16 of the 23 (70%) repeat biopsies. All infants were given an elemental diet (ED). Twelve of the 30 infants required parenteral nutrition (PN). These infants were gradually advanced to an oral elemental diet and maintained on this diet until histologic findings and disaccharidase levels were normal. Eighteen infants were fed and maintained on an elemental diet by mouth from time of admission until normal histologic findings and disaccharidases were found. No mortality occurred during management and follow-up. Twenty-two of the 28 infants in whom follow-up growth data were available excelled in weight and height velocity. The data suggest that prolonged injury to the small intestinal mucosa is a common finding in many cases of intractable diarrhea of infancy. Elemental diets should be started early in the course of protracted diarrhea in young infants, and may need to be continued for several months since histologic and enzymatic changes of the small intestine may persist for extended periods.
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PMID:Extent and duration of small intestinal mucosal injury in intractable diarrhea of infancy. 677 76

There are at least 20 rare autosomal recessive disorders that are excessively common in Finland of which congenital lactase deficiency is one. During the last 17 years we have found 16 cases. In each case the mother noted watery diarrhoea, generally after the first feed of breast milk, and at the latest, by age 10 days. The lactose malabsorption was verified at a mean age of 36 (range 3-90) days, by which time the infants were dehydrated and 15 of them weighed less than at birth (mean weight for age was -2.8 SDs). On a lactose-free elimination diet (a group of 6 on Nutramigen and a group of 10 on soy-based formula) the children caught up in growth. One infant in each group showed allergic symptoms. While the infants were being breast fed their faeces contained 20 to 80 g/l lactose. In 24 peroral lactose tolerance tests, the greatest rise in blood glucose concentration was 0.8 mmol/l. Only 2 patients showed abnormal absorption when tested within a week of lactose elimination, and in each absorption tests became normal during the elimination period. Slight to partial villous atrophy of the jejunum was present in 4 early specimens, but in later ones the mean villous height was normal. The mean height of the epithelial cells was reduced and there were fewer intraepithelial lymphocytes in patients. The lactase activities in jejunal biopsy specimens were lower than in most patients with acquired lactase deficiency, with some overlap. The maltase and sucrase activities were normal.
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PMID:Congenital lactase deficiency. A clinical study on 16 patients. 684 26

Investigations by scanning electron microscopy into changes of surface morphology of small bowel mucosa in children with chronic nonspecific diarrhea are reported. The study population comprised 56 patients, ranging in age from 5 months to 7 years; 65% were between 10 and 28 months old, and 64% of the patients were boys. The major findings were: microorganisms on the mucosal surface; excessive extrusion of cell cytoplasm and of enterocytes (cell shedding); presence of excessive mucus on the mucosal surface; damage to the brush border; and partial villous atrophy. The latter lesion was found in only four patients. All these changes are considered pathologic and, for the most part, are presumed to be due to the presence of antigens, in particular, microorganisms. A depression of disaccharidase activities was encountered in 64% of the patients, but prevalence was without regard to age. Most common was a combined depression of lactase, sucrase, and maltase, as well as an isolated depression of lactase. The possibility has to be considered that enteroadherent microorganisms which are usually not considered pathogenic, and microorganisms such as Mycoplasma, may emerge as intestinal pathogens in susceptible children. It is feasible that genetic traits of the host and environmental factors facilitate adherence and colonization of the small bowel mucosa which, in turn, produces chronic diarrhea. Further studies are needed to confirm the preliminary information contained in this report.
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PMID:Chronic nonspecific diarrhea in children: investigation of the surface morphology of small bowel mucosa utilizing the scanning electron microscope. 688 51

The paper is concerned with the results of morphological and biochemical studies of the duodenum and ileum in young rabbits with salmonellosis. It was shown that all the parts of the small intestine were involved into the pathological process. Enzymopathy developed in the presence of acute catarrhal inflammation and erosive enteritis accompanied by ulceration of necrotized lymph follicles of Peyer's patches of the small intestine. The activity of maltase and alkaline phosphatase was found to be most vulnerable. Of crucial significance in the development of diarrhea in experimental young rabbits were pronounced morphological alterations and derangement of enzyme-forming function in the small intestine.
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PMID:[State of the small intestine in rabbits with salmonella infections]. 703 5

The efficacy of the new intestinal alpha-glucosidase inhibitor, miglitol, and glibenclamide were compared in a 6-month double-blind controlled protocol involving 100 non-insulin dependent diabetic patients under diet alone. HbA1c levels (initially between 7 and 11%) were reduced (p < 0.05): -0.78 +/- 0.21% after miglitol and -1.18 +/- 0.20% after glibenclamide. The difference between the two treatments was not significant, although glibenclamide appeared to be more active than miglitol at 8 (p = 0.002) and 16 weeks (p = 0.01) but not at 24 weeks. Fasting glycaemia decreased after miglitol (8.7 +/- 0.3 vs 9.6 +/- 0.3 mmol/l, p = 0.005) and after glibenclamide (8.0 +/- 0.3 vs 9.1 +/- 0.3, p = 0.007). After miglitol, a decrease was noted after breakfast (p < 0.001) and lunch (p < 0.001). The same was true for glibenclamide (p = 0.004 and p < 0.001 respectively). A significant reduction in glucose incremental area during a standard meal test was noted at the end of miglitol (p = 0.008) or glibenclamide treatment (p = 0.04). Subgroups of nonresponders to both treatments were identified (10/49 with miglitol, 9/47 with glibenclamide). Side effects were recorded in 10 patients treated with miglitol (flatulence and meteorism, diarrhoea, 1 discontinued therapy) and in 10 treated with glibenclamide (asthenia, sensation of hunger). This study indicates that miglitol is suitable for initial application in diet-resistant Type 2 diabetic patients, providing, a persistent effect and acceptable side effects.
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PMID:Comparison of miglitol and glibenclamide in diet-treated type 2 diabetic patients. 755 6

Two experiments were conducted to determine intestinal disaccharidase activity in 1-day-old commercial turkey poults inoculated with astrovirus. Small intestinal samples were collected on days 0.5, 1, 3, and 7 postinoculation (PI) in Expt. 1 and on days 7, 10, and 14 PI in Expt. 2 and evaluated for specific maltase activity (SMA). Astrovirus infection was verified on day 7 PI by immune electron microscopy of intestinal contents. Inoculated poults developed diarrhea and a transient, significant decrease in intestinal SMA. SMA was significantly (P < 0.05) lower in astrovirus-inoculated poults than in control poults throughout the entire small intestine from day 3 through day 7 PI. However, SMA had returned to normal in inoculated poults by day 10 PI and was significantly higher than control values (P < 0.05) in all sections of the small intestine, except in the proximal jejunum, by day 14 PI. Decreased SMA caused by astrovirus infection resulted in disaccharide maldigestion, malabsorption, and subsequent osmotic diarrhea. As astrovirus was cleared from the intestinal tract, SMA was restored and diarrhea was resolved.
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PMID:Astrovirus infection in hatchling turkeys: alterations in intestinal maltase activity. 767 56

The 4-5 days-old NMRI strain infant mice were orally inoculated with EB rotavirus (serotype 3). The intestinal disaccharidases activity was studied separately in three segments of the small intestine i.e. duodenum, jejunum and ileum on day 1 to 7 post inoculation (p.i.). The severity of EB rotavirus infection correlated with a significant decrease of small intestinal lactase, maltase and sucrase on day 3 p.i. The level of maltase after the initial decline increased in all the three segments of small intestine of infected mice. However, the lactase activity remained suppressed for a relatively longer period in ileum of infected mice than in controls. These enzymes began to approach to normal value by day 5 p.i., but in ileum, lactase activity continued to be severely depressed even on day 7 p.i. Rotavirus was consistently detected in intestinal contents by ELISA on days 1 to 7 p.i. The infected mice showed a significant increase in rotavirus (serotype 3)-specific serum IgG and IgM antibody level during the declining (days 5-7 p.i.) phase of infection. Diarrhoea was noted up to day 6 p.i. The protracted suppression of the lactase activity in ileum in comparison to duodenum and jejunum showed a differential tropism of EB rotavirus (serotype 3) strain to the small intestine of homologous murine model.
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PMID:Differential tropism of EB rotavirus (serotype 3) to small intestine of homologous murine model. 772 1

Acarbose is an alpha-glucosidase inhibitor proposed for the treatment of diabetic patients. It acts by competitively inhibiting the alpha-glucosidases in the intestinal brush border. The principal action of these enzymes is to convert nonabsorbable dietary starch and sucrose into absorbable monosaccharides (e.g. glucose). Enzyme inhibitors delay this conversion, slowing the formation and consequently the absorption of monosaccharides, and thus reducing the concentration of postprandial blood glucose. Both starch and sucrose are influenced, whereas lactose and glucose are not. Many studies in experimental animals, healthy volunteers and patients with non-insulin-dependent diabetes mellitus (NIDDM) have shown that acarbose decreases postprandial blood glucose, with a lesser reduction of fasting blood glucose, plasma triglycerides and postprandial insulin levels. In long term studies in NIDDM patients, acarbose significantly reduced glycosylated haemoglobin levels. Acarbose is only minimally absorbed from the gut and no systemic adverse effects have been demonstrated after long term administration. The drug allows undigested carbohydrates to pass into the large bowel where they are fermented causing flatulence, bloating and diarrhoea. These symptoms, which occur in approximately 30 to 60% of patients, tend to decrease with time and seem to be dose-dependent. They are minimised by starting therapy with low doses (such as 50mg 3 times daily) which may be effective in many patients. An increase in serum hepatic transaminases observed in earlier studies in the US, where doses of acarbose up to 900mg daily were used, has been not reported with the lower doses of the drug actually recommended [150 to 300mg (up to 600mg) daily]. In conclusion, acarbose may be useful in patients with NIDDM when diet alone is no longer able to maintain satisfactory blood glucose control. Furthermore, it may be a valid alternative to sulphonylurea or biguanide therapy when these drugs are contraindicated and insulin administration may be delayed. Acarbose seems also to be a useful adjunct to hypoglycaemic oral agents but its precise role in this field has not been fully clarified.
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PMID:A risk-benefit appraisal of acarbose in the management of non-insulin-dependent diabetes mellitus. 772 53

We conducted a double-blind, randomized phase II study to evaluate the safety and activity of combination therapy with N-butyl-deoxynojirimycin (SC-48334) (an alpha-glucosidase I inhibitor) and zidovudine versus zidovudine alone. Patients with 200 to 500 CD4 cells/mm3 who tolerated < or = 12 weeks of prior zidovudine therapy received SC-48334 (1000 mg every 8 h) and zidovudine (100 mg every 8 h) or zidovudine and placebo. Sixty patients received combination therapy and 58, zidovudine and placebo. Twenty-three patients (38%) and 15 (26%), in the combination and zidovudine groups, respectively, discontinued therapy (p = 0.15). The mean SC-48334 steady-state trough level (4.04 +/- 0.99 micrograms/ml) was below the in vitro inhibitory concentration for human immunodeficiency virus (HIV). The mean increase in CD4 cells at week 4 was 73.8 cells/mm3 and 52.4 cells/mm3 for the combination and zidovudine groups, respectively (p > 0.36). For patients with prior zidovudine therapy, the mean change in CD4 cells in the combination and zidovudine groups was 63.7 cells/mm3 and 4.9 cells/mm3 at week 8 and 6.8 cells/mm3 and -45.1 cells/mm3 at week 16, respectively. The number of patients with suppression of HIV p24 antigenemia in the combination and zidovudine groups was six (40%) and two (11%) at week 4 (p = 0.10) and five (45%) and two (14%) at week 24 (p = 0.08), respectively. Diarrhea, flatulence, abdominal pain, and weight loss were common for combination recipients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety and efficacy of combination N-butyl-deoxynojirimycin (SC-48334) and zidovudine in patients with HIV-1 infection and 200-500 CD4 cells/mm3. 790 23

Sulfites are usually added to food, beverages and pharmaceuticals as preservative antioxidants, bleaching agents, and dough conditioning agents. Ingestion of foods containing sulfites can cause abdominal pain, diarrhoea, seizures and death. Sulfite can react with cellular components and can cause toxicity. Changes in mucosal disaccharidases and phosphatase alkaline after sodium metabisulfite administration were investigated in the small intestine of rats. Female Wistar rats were given a diet supplemented with 0.25 or 2.5% sodium metabisulfite for 5 weeks. Sucrase, maltase, lactase and alkaline phosphatase were assayed in intestinal homogenates and in brush border membrane fractions. The intake of only 2.5% sulfite induced an increase in the specific activities of sucrase, maltase, and alkaline phosphatase compared to control levels (P < 0.05). Lactase levels were affected in a variable manner. The origin of such altered enzyme activities is still unknown.
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PMID:Effect of sulfite intake on intestinal enzyme activity in rats. 795 44


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