Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Saccharomyces boulardii (S.b.) is used for the prevention and treatment of diarrhea of different etiologies. We prospectively investigated the effects of S.b. on lymphocytes and duodenal mucosa. Before and after oral administration of S.b. for 3 weeks, circulating and intestinal lymphocytes were isolated and characterized by flow cytometry. Trophic effects on duodenal mucosa were investigated by morphometry and determination of brush border enzyme activity. Results were compared intraindividually before and after S.b. In intestinal lymphocytes no phenotypic changes were observed. CD4+ cells of the peripheral blood had a significantly increased expression of CD25 (p < 0.02). None of twelve volunteers had an increase in villous surface area (n.s.). Immunoglobulin A content in small intestine secretion was unaltered. An increase in brush border enzyme activity of lactase, alpha-glucosidase, and alkaline phosphatase was observed (p < 0.01). Our findings indicate that S.b. has a positive effect on the maturation of enterocytes and only a minor influence on lymphocytes.
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PMID:Immunological and trophical effects of Saccharomyces boulardii on the small intestine in healthy human volunteers. 878 7

Two studies were conducted to investigate whether vitamin A-deficient rats were more susceptible to intestinal injury caused by methotrexate (MTX), since vitamin A deficiency alone causes only mild changes to jejunal structure and function. Weanling male rats were fed a vitamin A-deficient diet (-VA) for 40-42 d and compared to rats either pair-fed (PF) or with free access (+VA) to the same diet. Drinking water of PF and +VA rats was supplemented with 37.5 microg (Study 1) or 75 microg (Study 2) vitamin A (Rovimix A 500W)/d. Rats in each group received MTX (-VAMTX, PFMTX, +VAMTX) or vehicle. MTX administration reduced intestinal mucosal wet weight, protein and DNA concentrations, and sucrase and maltase activities in -VA and PF rats (P < 0.02). In Study 1, -VAMTX rats developed a severe jejunal enteropathy and had a higher incidence of diarrhea (P < 0.005), greater weight loss (P < 0.005), more disruption of villus architecture (P < 0.0001) and lower disaccharidase activity (P < 0.007) than PFMTX rats. Similar results were observed in Study 2. Liver retinol concentration (but no other variable) was greater in rats receiving 75 microg vitamin A/d (P < 0.001) than in those receiving 37.5 microg/d. The interaction of vitamin A deficiency and small intestinal injury may explain the efficacy of vitamin A supplementation in preventing childhood diarrheal disease mortality in developing countries, and highlights the need for ensuring adequate vitamin A status in people worldwide with diseases and/or treatments which may injure the gastrointestinal tract.
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PMID:Vitamin A deficiency exacerbates methotrexate-induced jejunal injury in rats. 916

Stunting syndrome (SS) is an enteric disease of turkey poults that causes high morbidity including reduced growth, impaired feed efficiency, and diarrhea. The etiologic agent of this disease has not been previously reported. The objectives of the present study were to identify, isolate, and purify the etiologic agent of SS. Day-old poults were orally inoculated with a SS-inducing inoculum. The intestinal epithelial cells (IECs) were isolated on the fourth day postinoculation. The IECs were lysed and filtered through 0.2-, 0.1-, and 0.02-micron filters. The cell lysate filtrate (0.1 micron) was subjected to density gradient ultracentrifugation. Intact IECs, filtrates from IECs (0.2, 0.1, and 0.02 micron ), and IEC lysate fractions from gradients (FRG) were used as inocula to infect day-old turkey poults. The weight gain, jejunal maltase activity, and gross intestinal lesions were used as the parameters of evaluation. Weight gain and maltase activity were reduced (P = 0.001) by the isolated IECs, 0.2 and 0.1 micron filtrates, and FRG when compared with corresponding controls. IEC lysate filtrate (0.1 micron) and FRG were examined under transmission electron microscope (EM). Enveloped, pleomorphic particles varying in size from 60 to 95 nm were observed and termed stunting syndrome agent (SSA). Primary cultures of turkey IECs were used to further isolate and propagate the SSA. Following the fifth passage in the turkey IECs, the cell lysate induced SS in day-old poults. SSA particles were observed under EM after the fifth passage. The results of this study provide evidence that a viral agent has been isolated and identified from IECs of SS-infected poults and is the etiologic agent of SS.
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PMID:Stunting syndrome in turkey poults: isolation and identification of the etiologic agent. 945 21

The objective of this study was to determine the safety, efficacy, and tolerability of the alpha-glucosidase inhibitor miglitol vs. the sulfonylurea glyburide in the treatment of elderly patients with type 2 diabetes mellitus, inadequately controlled by diet alone. This was a double-blind, randomized, placebo-controlled, 1-yr trial of miglitol 25 mg TID and 50 mg TID compared with placebo and a titrated dose of glyburide in a parallel group comparison study conducted in 30 out-patient sites across the United States. Four hundred eleven (411) diet-treated patients age 60 yr or greater were randomized to receive either placebo TID (n = 101), miglitol 25 mg TID (n = 104), miglitol 50 mg TID (n = 102), or a once-daily dose of glyburide titrated based on fasting plasma glucose (FPG) (n = 104), for a period of 56 weeks. Efficacy was assessed by glycated hemoglobin (HbA1c), fasting and post-meal glucose, insulin, and lipid levels, and by 24-h urinary excretion of glucose and albumin. Safety and tolerability were assessed by tabulation of adverse events, periodic laboratory determinations, and home blood glucose monitoring. HbA1c treatment effects (placebo-subtracted change in HbA1c from baseline) at the 1-yr endpoint were -0.49%, -0.40%, and -0.92% in the miglitol 25 mg TID, miglitol 50 mg TID, and glyburide groups, respectively (P < 0.05- 0.01 vs. placebo). Postprandial insulin levels were significantly greater than placebo and miglitol in the glyburide group (P < 0.01). Hypoglycemia, weight gain, and both routine and serious cardiovascular events were more frequent in the glyburide group (P < 0.05-0.01 vs. placebo or miglitol groups). Diarrhea (or soft stools) and flatulence were more common in both miglitol groups than in the other two groups in a dose-dependent manner, but resulted in relatively few study dropouts. Treatment with miglitol offers the elderly type 2 diabetic patient significant reductions in daylong glycemia as measured by HbA1c. The greater HbA1c reductions seen with once-a-day glyburide occurred at a cost of significant increases in weight, insulin levels, and the incidences of clinical and subclinical hypoglycemia, which did not occur in the miglitol groups. alpha-glucosidase inhibitors are a useful and relatively safe therapeutic option in the elderly patient with type 2 diabetes.
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PMID:Advantages of alpha-glucosidase inhibition as monotherapy in elderly type 2 diabetic patients. 958 48

Escherichia coli heat-stable enterotoxin b (STb) causes severe diarrhoea in weaning piglets. STb most probably has to bind to intestinal epithelial cells in order to achieve its effect. Using biotinylated biologically active STb, we developed a semi-quantitative binding assay using indirect fluorescence microscopy. We demonstrated the attachment of the biotinylated toxin to microvilli of the pig jejunum. However, binding was abolished when biotinylated STb was either boiled or treated with 2-mercaptoethanol, treatments known to abolish biological activity. Different characteristics of STb attachment to the pig small intestine were determined. The reaction was rapid and reached maximum intensity after approximately 10 min. The binding was pH dependent showing an optimum at pH 5.8. Incubation at either 4 degrees C, 25 degrees C or 37 degrees C did not affect the binding. No competition was observed with non-biotinylated STb. However, preincubation of biotinylated STb with streptavidin conjugated to horseradish peroxidase completely abolished the binding. Pig tissues other than jejunum demonstrated binding towards STb including duodenum, ileum, caecum, colon, liver, lung, spleen and kidney. The molecule involved was then partially characterized. Metaperiodate treatment of the jejunum sections abrogated binding but protease treatment had no effect. Enzymatic treatments of jejunal sections demonstrated that N- and O-glycosidases, and several exoglycosidases did not affect binding, whereas reduced binding was observed with ceramide glycanase and alpha-glucosidase, and was completely abolished following neuraminidase treatment. Overall, our results suggest that in vitro STb binding was rapid, pH dependent, temperature independent, not restricted to jejunum and involves a molecule that seems to be composed of a ceramide moiety, terminal neuraminic acid and/or alpha-linked terminal glucose residue(s).
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PMID:Binding characteristics of Escherichia coli enterotoxin b (STb) to the pig jejunum and partial characterization of the molecule involved. 960 Aug 60

Acarbose is the first of a new class of antidiabetic agents, the alpha-glucosidase inhibitors. Acarbose has proven effectiveness as a first-line drug in type 2 diabetes insufficiently controlled by diet alone. In addition to providing short-term glycemic control, acarbose also reduces HbA1c levels. This effect is greatest when therapy is initiated early in the disease and when baseline HbA1c levels are high. Depending on the baseline HbA1c value, therapeutic doses of acarbose lead to a HbA1c reduction of 0.5%-1.2%. Acarbose may be safely combined with all oral hypoglycemic agents, and has been found to have utility as an adjunct to sulfonylurea and metformin therapy. It also improves control of insulin-treated type 2 diabetes and enables a reduction of exogenous insulin requirements of up to 30%. Acarbose also has beneficial effects on the coronary risk factors, e.g. postprandial triglyceride levels, elevated cholesterol, and hyperinsulinemia. The early phase of acarbose therapy may be associated with side effects such as meteorism, flatulence, and diarrhea. These result from the local effect of the drug and decline with time. To date, there have been no reports of systemic toxicity. Acarbose does not cause hypoglycemias or weight gain.
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PMID:The role of acarbose in the treatment of non-insulin-dependent diabetes mellitus. 964 42

The increased intestinal absorption induced by epidermal growth factor (EGF) is associated with diffuse lengthening of brush border microvilli. The aim of this study was to examine the in vivo effects of oral administration of EGF during infection with enteropathogenic Escherichia coli. New Zealand White rabbits (4 weeks old) received orogastric EGF daily starting 3 days prior to infection with enteropathogenic E. coli RDEC-1 and were compared with sham-treated infected animals and uninfected controls. Weight gain, food intake, fecal E. coli, and stool consistency were assessed daily. On day 10, segments of jejunum, ileum, proximal, and distal colon were assessed for gram-negative bacterial colonization, disaccharidase activities, and epithelial ultrastructure. Effects of EGF on E. coli RDEC-1 proliferation were studied in vitro. E. coli RDEC-1 caused diarrhea and reduced weight gain. Seven days postinfection, the small and large intestines were colonized with numerous bacteria, brush border microvilli were disrupted, and maltase and sucrase activities were significantly reduced in the jejunum. Daily treatment with EGF prevented the occurrence of diarrhea and reduction of weight gain. These effects were associated with significant inhibition of E. coli colonization in the small and large intestine, improved jejunal maltase and sucrase activities and reduced microvillous injury. EGF did not affect the proliferation of E. coli in vitro. The findings suggest that EGF protects the gastrointestinal tract against colonization by enteropathogenic E. coli.
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PMID:Effects of orally administered epidermal growth factor on enteropathogenic Escherichia coli infection in rabbits. 974 97

The drugs used to treat diabetes mellitus are diverse and involve several classes. However, these drugs can be roughly separated into hypoglycaemic agents, such as insulin and the sulphonylureas, and antihyperglycaemic agents, such as the biguanides, the alpha-glucosidase inhibitors and troglitazone. Reports of insulin overdose are rare. The major effects of insulin overdose are secondary to the insult to the CNS produced by hypoglycaemia. The mainstay of insulin overdose management is glucose replacement therapy. Sulphonylureas are the most commonly used oral antihyperglycaemic agents in the management of type 2 (non-insulin-dependent; NIDDM) diabetes mellitus. Sulphonylureas primarily cause serum glucose reduction by stimulating the release of preformed insulin from the pancreatic islets. The mainstay of sulphonylurea overdose management is glucose replacement therapy, and in severe cases, reduction of insulin release. In the large majority of patients intravenous glucose supplementation will be sufficient to maintain euglycaemia. Repaglinide, a meglitinide analogue, is a new nonsulphonylurea oral hypoglycaemic agent. In overdose, this drug may produce prolonged hypoglycaemia similar to the sulphonylureas. The primary problem with biguanide overdose is the potential for lactic acidosis. The management of biguanide overdose is largely supportive and directed at correcting the metabolic acidosis along with associated complications. The alpha-glucosidase inhibitors, acarbose, voglibose and miglitol competitively and reversibly inhibit the alpha-glucosidase enzymes (glucoamylase, sucrase, maltase and isomaltase) in the brush border in the small intestine, which delays the hydrolysis of complex carbohydrates. They appear unlikely to produce hypoglycaemia in overdose, but abdominal discomfort and diarrhoea may occur. Troglitazone is the first thiazolidinedione antidiabetic drug available. There are no data on overdose, probably because of its very recent introduction. Overdoses with antidiabetic drugs produce major morbidity, with many cases requiring intensive care medicine and prolonged hospital stays. However, fatalities are rare when treatment is initiated early. The management of the hypoglycaemic drugs (insulin and sulphonylureas) is based primarily on restoring and maintaining euglycaemia via intravenous dextrose supplementation. In the case of the sulphonylureas, reduction of insulin secretion via pharmacological intervention may also be necessary. With biguanides the main risk appears to be cardiovascular collapse secondary to profound acidosis. The management focus is on restoring acid-base balance with hyperventilation and the use of insulin to shift the utilisation of glucose from the nonoxidative pathway to the oxidative pathway. Use of haemodialysis has shown equivocal results but may be valuable in metformin overdose.
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PMID:Management of antidiabetic medications in overdose. 982 53

Diarrhoea is a relatively frequent adverse event, accounting for about 7% of all drug adverse effects. More than 700 drugs have been implicated in causing diarrhoea; those most frequently involved are antimicrobials, laxatives, magnesium-containing antacids, lactose- or sorbitol-containing products, nonsteroidal anti-inflammatory drugs, prostaglandins, colchicine, antineoplastics, antiarrhythmic drugs and cholinergic agents. Certain new drugs are likely to induce diarrhoea because of their pharmacodynamic properties; examples include anthraquinone-related agents, alpha-glucosidase inhibitors, lipase inhibitors and cholinesterase inhibitors. Antimicrobials are responsible for 25% of drug-induced diarrhoea. The disease spectrum of antimicrobial-associated diarrhoea ranges from benign diarrhoea to pseudomembranous colitis. Several pathophysiological mechanisms are involved in drug-induced diarrhoea: osmotic diarrhoea, secretory diarrhoea, shortened transit time, exudative diarrhoea and protein-losing enteropathy, and malabsorption or maldigestion of fat and carbohydrates. Often 2 or more mechanisms are present simultaneously. In clinical practice, 2 major types of diarrhoea are seen: acute diarrhoea, which usually appears during the first few days of treatment, and chronic diarrhoea, lasting more than 3 or 4 weeks and which can appear a long time after the start of drug therapy. Both can be severe and poorly tolerated. In a patient presenting with diarrhoea, the medical history is very important, especially the drug history, as it can suggest a diagnosis of drug-induced diarrhoea and thereby avoid multiple diagnostic tests. The clinical examination should cover severity criteria such as fever, rectal emission of blood and mucus, dehydration and bodyweight loss. Establishing a relationship between drug consumption and diarrhoea or colitis can be difficult when the time elapsed between the start of the drug and the onset of symptoms is long, sometimes up to several months or years.
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PMID:Drug-induced diarrhoea. 1064 76

The use of probiotics to enhance intestinal health has been proposed for many years. Probiotics are traditionally defined as viable microorganisms that have a beneficial effect in the prevention and treatment of specific pathologic conditions when they are ingested. There is a relatively large volume of literature that supports the use of probiotics to prevent or treat intestinal disorders. However, the scientific basis of probiotic use has been firmly established only recently, and sound clinical studies have begun to be published. Currently, the best-studied probiotics are the lactic acid bacteria, particularly Lactobacillus sp. and Bifidobacterium sp. However, other organisms used as probiotics in humans include Escherichia coli, Streptococcus sp., Enterococcus sp., Bacteroides sp., Bacillus sp., Propionibacterium sp. and various fungi. Some probiotic preparations contain mixtures of more than one bacterial strain. Probiotics have been examined for their effectiveness in the prevention and treatment of a diverse spectrum of gastrointestinal disorders such as antibiotic-associated diarrhea (including Clostridium difficile-associated intestinal disease), infectious bacterial and viral diarrhea (including diarrhea caused by rotavirus, Shigella, Salmonella, enterotoxigenic E. coli, Vibrio cholerae and human immunodeficiency virus/acquired immunodeficiency disorder, enteral feeding diarrhea, Helicobacter pylori gastroenteritis, sucrase maltase deficiency, inflammatory bowel disease, irritable bowel syndrome, small bowel bacterial overgrowth and lactose intolerance. Probiotics have been found to inhibit intestinal bacterial enzymes involved in the synthesis of colonic carcinogens. There are many mechanisms by which probiotics enhance intestinal health, including stimulation of immunity, competition for limited nutrients, inhibition of epithelial and mucosal adherence, inhibition of epithelial invasion and production of antimicrobial substances. Probiotics represent an exciting prophylactic and therapeutic advance, although additional investigations must be undertaken before their role in intestinal health can be delineated clearly.
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PMID:The role of probiotic cultures in the control of gastrointestinal health. 1072 14


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