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)

The 1,4-alpha-glucosidase inhibitor. Acarbose, when injected intraperitoneally disturbs liver lysosome metabolism, causing distinct and persistent inhibition of the enzymes and acute disturbances of lysosomal glycogen metabolism. A feedback control mechanism appears to operate, affecting cytosolic carbohydrate metabolism. A model is suggested for the adult form of lysosomal storage disease. The biochemical effects closely resemble those occurring in glycogenosis type II (Pompe's disease), and these have been confirmed by electron microscopy.
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PMID:Lysosomal glycogen storage induced by Acarbose, a 1,4-alpha-glucosidase inhibitor. 389 20

Rats with a gentic deficiency of phosphorylase kinase have been treated with the 1,4-alpha-glucosidase inhibitor, Acarbose. Lysosomal glycogen metabolism has been markedly altered and the results support the concept of a feedback control mechanism operating on the uptake mechanism into the lysosomal compartment.
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PMID:Factors affecting the metabolic control of cytosolic and lysosomal glycogen levels in the liver. 389 36

Acarbose is an alpha-glucosidase inhibitor which reversibly and competitively inhibits the digestion of oligo- and disaccharides at the brush border of the small intestine. This study evaluates the preventive and therapeutic properties of acarbose in the treatment of obesity. Dose-response experiments were performed during repeated sucrose loads in man in order to investigate the effects of acarbose on plasma insulin and blood glucose levels. After titration of efficient doses, a long-term tolerance test of acarbose was undertaken in a small pilot study. Finally, the relapse preventing effect of acarbose was tested during double-blind cross-over conditions in 24 weight reduced obese women. In growing Sprague-Dawley rats, the effects of acarbose on body weight, lipid depots and adipose tissue cellularity were tested during pair-feeding and ad libitum conditions. Such effects were also studied in adult ad libitum-fed rats. Blood glucose, plasma insulin, body fat, depot lipids as well as fat cell weight and number were determined with established techniques. During a sucrose load, acarbose reduced insulin in a dose-dependent fashion. Glucose was also reduced, but not dose-dependently and only to a moderate extent. During a 200 g sucrose load, 400 mg of acarbose did not necessarily result in a maximal reduction of the insulin response while the glucose response was maximally inhibited after 100 mg. Acarbose reduced the relapse rate after weight reduction. No serious side effects were observed. Flatulence and meteorism occurred frequently. In growing rats, acarbose retarded the development of body weight and of lipid depots not only during pair-feeding conditions but also in ad libitum-fed animals eating considerably more than their controls. The spontaneous food consumption was increased by acarbose also in adult rats but in these animals neither body weight nor lipid depots were significantly reduced by acarbose. It is concluded that acarbose induces a carbohydrate malabsorption. Insulin levels are reduced not only via a decreased glycemic stimulus but also by interference with other insulin releasing mechanism(s). Acarbose is the first drug ever tested with long-term relapse reducing effects after weight reduction. Animal experiments suggest that acarbose may be of value in the prevention of obesity, particularly since the drug retards lipid accumulation also during ad libitum-feeding.
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PMID:alpha-Glucosidase inhibition in obesity. 391 27

The present paper describes an animal model of lysosomal glycogenosis as induced by a competitive inhibitor of alpha-glucosidase. Rats received intraperitoneal injections of the inhibitor, a pseudotetrasaccharide (Acarbose, Bay g 5421); liver tissue was examined by light and electron microscopy. Substrate-histochemical and enzyme-cytochemical methods were used to demonstrate intralysosomal glycogen storage within hepatocytes and Kupffer cells. The cytological picture closely resembled that occurring in glycogenosis type II (Pompe's disease) of humans. After cessation of drug treatment, the glycogen storage was slowly reversible. The present results point to the physiological role of the lysosomal apparatus for intracellular glycogen turnover. On the cellular level, this experimentally induced glycogenosis may be useful as a model of Pompe's disease.
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PMID:Lysosomal glycogen storage mimicking the cytological picture of Pompe's disease as induced in rats by injection of an alpha-glucosidase inhibitor. I. Alterations in liver. 611 39

The effects of sucrose and Acarbose (alpha-glucosidase inhibitor) feeding on the development of diabetes were studied in streptozotocin-treated rats. Rats were raised on four different dietary regimens, viz, a sucrose diet (46% of the total weight in the form of sucrose, 24% as starch), a starch diet (70% as starch), a standard diet (laboratory chow: Oriental Yeast Co.) or an Acarbose diet (a standard diet containing 75 mg Acarbose/100g diet) for a week followed by an intraperitoneal injection of streptozotocin (70 mg/kg). Development of diabetes was determined by urinary and blood glucose levels (more than 250 mg/dl). The incidence of diabetes in the groups of rats fed on sucrose, starch, standard, and Acarbose diets was 100%, 80%, 70% and 47.6%, respectively. The development of diabetes was accelerated by sucrose feeding and depressed by Acarbose feeding. There was mild diabetes in rats fed on Acarbose diet. The sucrose feeding caused a marked increase of disaccharidase activities in the proximal part of the intestine and in the apical part of the villus-crypt gradient of epithelial cells. The Acarbose feeding caused a significant decrease of disaccharidase activities. The changes in protein content of the sucrase-isomaltase complex appeared to be in parallel with those of disaccharidase activities. These results suggest that intestinal disaccharidase activities are involved in the development of experimental diabetes induced by streptozotocin.
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PMID:Effect of sucrose and Acarbose feeding on the development of streptozotocin-induced diabetes in the rat. 621 54

Acarbose is known to inhibit glucoamylase, maltase and sucrase. Our aim was to test whether it would also inhibit glucosyltransferase (GTF), to determine the type of inhibition and to compare the inhibitor potency of acarbose with that of nojirimycin and deoxynojirimycin, two other glucosidase inhibitors. Enzyme inhibition was measured either by chemical assay or by incorporation of radioactivity into product. Acarbose effectively inhibited the synthesis of polysaccharide by GTF from strains of Streptococcus mutans and Streptococcus sanguis, but not by fructosyltransferase from Streptococcus salivarius. Acarbose and 1-deoxynojirimycin were more potent inhibitors of GTF than maltose, nojirimycin or various amino sugars. The mechanism of action of these compounds is consistent with competitive inhibition.
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PMID:Inhibition by acarbose, nojirimycin and 1-deoxynojirimycin of glucosyltransferase produced by oral streptococci. 622 60

Glucose and insulin responses to a standardized test meal in patients with chronic duodenal ulceration were measured pre-operatively and again post-operatively. An abnormal pre-operative glucose tolerance contributes to an even more deranged post-operative glucose tolerance. However, following administration of an alpha-glucosidase inhibitor, Acarbose, these post-operative abnormalities are markedly attenuated.
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PMID:Glucose and insulin levels in duodenal ulcer disease before and after surgery. 635 9

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemic excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose [(1-14C]glucose and a simultaneous intravenous infusion of [3-3H]glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemic excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.
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PMID:The effects of an alpha-glucoside hydrolase inhibitor on glycemia and the absorption of sucrose in man determined using a tracer method. 636 57

Effects of either a single dose or a long-term administration of an alpha-glucosidase inhibitor, acarbose, on blood glucose, cholesterol concentrations in serum lipoprotein fractions, triglycerides and free fatty acids were examined in streptozotocin-induced diabetic rats. In experiment 1, starch loading tests were performed with or without adding acarbose. The addition of acarbose (0.75 mg per kg of body weight or over) significantly reduced the elevation of blood glucose levels. In experiment 2, the animals were divided into three groups: Group A fed on a control diet, Group B fed on a diet containing 5 mg acarbose in 100 g of diet and Group C fed on a diet containing 20 mg acarbose in 100 g of diet. The food intake in Group C was significantly reduced by 22% as compared to Group A, while the food intake in Group B showed no change. The high dose of acarbose showed a tendency to lower fasting blood glucose levels, but the difference was statistically insignificant. However, postprandial glucose levels in Group C at each period examined and in Group B at 30 days were significantly lower than the counterparts in Group A. Acarbose caused a dose-dependent decrease in serum total cholesterol levels and HDL-cholesterol: total cholesterol ratios were elevated in Group B and C. Serum triglyceride levels in Group B and C were extremely lower than those in Group A on and after 20 days. These results indicate that the addition of acarbose to the diet induces a decrease in postprandial blood glucose levels and simultaneously causes an improvement in lipid metabolism of streptozotocin-induced diabetic rats.
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PMID:Effects of an alpha-glucosidase inhibitor, acarbose, on blood glucose and serum lipids in streptozotocin-induced diabetic rats. 637 45

In rats, the period of refeeding after a fast is associated with accelerated weight gain without a concomitant increase in food intake. In this study the alpha-glucosidase inhibitor, acarbose, was used to delay carbohydrate absorption in normal adult rats, and the effects on body weight, food intake, and intestinal enzyme activities were determined. Refeeding with acarbose in the food (500 mg/kg) reduced the rate of weight gain compared to refeeding without acarbose but did not change food intake. Acarbose also lowered midjejunal mass and blunted the refeeding-induced rise in certain brush border disaccharidase and intracellular glycolytic enzymes. However, acarbose refed rats still had accelerated weight gain compared to nonfasted rats, implying that the refeeding response was not totally abolished. These studies suggest that inhibition of carbohydrate absorption during refeeding might have a role in the maintenance of diet-induced weight loss.
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PMID:Modification of weight gain by an alpha-glucosidase inhibitor during refeeding in rats. 638 Feb 64


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