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)

Acarbose, an alpha-glucosidase inhibitor, delays absorption of carbohydrate in the gut, thereby lowering postprandial glucose levels. Safety data on this drug have been gathered in a series of studies on animals and in extensive clinical trials in humans. Although an initial long term feeding study in rats showed an excess of renal tumours at very high dosages of acarbose (up to 300 mg/kg bodyweight daily), further evaluation with similar studies in rats, hamsters, and dogs indicated that the problem was related to carbohydrate malabsorption. With adequate glucose intake and in gavage studies, no difference in tumour incidence between placebo- and acarbose-treated groups was seen. From 1976 to 1989, safety data on acarbose were obtained in approximately 8800 patients in 2 separate groups of clinical trials, the Bayer International Clinical Data Pool and the American phase III trials. Almost all adverse experiences, as reported by 56 to 76% of patients on acarbose vs 32 to 37% of patients on placebo, were related to the digestive system and included diarrhoea, flatulence, bloating and nausea. Most symptoms were of mild to moderate intensity and tended to improve with time. In the American trials a small but significant increase in liver transaminases was seen, 3.8% in acarbose-treated patients vs 0.9% in controls together with a 1% increase in anaemia in the acarbose group. Overall, acarbose was well tolerated and the adverse experience profile was clinically acceptable.
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PMID:Safety profile of acarbose, an alpha-glucosidase inhibitor. 128 May 77

Metabolic studies are described in a patient who presented at 3 weeks of age with severe anaemia, hyperbilirubinaemia and hypotonicity. Clinically, glycogen storage disease type II (Pompe disease) was suspected because of a massively enlarged heart and hepatosplenomegaly. This was confirmed biochemically by the demonstration of glycogen accumulation in skeletal muscle and undetectable acid alpha-1,4-glucosidase activity in fibroblasts. Further biochemical studies in this patient surprisingly revealed homocystinuria and methylmalonic aciduria, suggesting a defect in the uptake, transport or intracellular metabolism of vitamin B12. Studies in cultured fibroblasts from the patient revealed a low uptake of [57Co]cyanocobalamin and an impaired intracellular conversion to both 5'-deoxyadenosylcobalamin and methylcobalamin. Moreover, the incorporation of labelled propionate into proteins as well as the formation of labelled methionine from labelled 5-methyltetrahydrofolate was deficient in fibroblasts from the patient. Complementation studies revealed the presence of the cblC mutation in this patient. No treatment was initiated and the patient died at the age of 31 days. We conclude that the patient was affected by both glycogen storage disease type II and cblC disease. The remarkable combination of these two rare inborn errors can be the result of the consanguinity of the parents.
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PMID:Clinical and biochemical observations in a patient with combined Pompe disease and cblC mutation. 153 54

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.
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PMID:Disaccharidase levels in iron deficient rats at birth and during the nursing and postweaning periods: response to iron treatment. 707 2

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.
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PMID:Disaccharidase levels in normal epithelium of the small intestine of rats with iron-deficiency anemia. 936 8

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.
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PMID:Relation of the disaccharidases in the small intestine of the rat to the degree of experimentally induced iron-deficiency anemia. 1077 85