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Precose

Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Other names for this medication:

Similar Products:
Glucophage, Actos, Avandia, Amaryl, Glucovance, Micronase, Glycomet

 

Also known as:  Acarbose.

Description

Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Generic Precose is a glucosidase inhibitor. It works by slowing down the enzyme that turns carbohydrates into glucose; it decreases blood sugar levels following a meal.

Precose is also known as Acarbose, Glucobay, Glucor, Rebose.

Generic name of Generic Precose is Acarbose.

Brand name of Generic Precose is Precose.

Dosage

Take Generic Precose by mouth with food.

If you also take charcoal or digestive enzyme preparations, do not take them within 2 to 4 hours before after taking Generic Precose.

Temporary insulin therapy may be necessary during stressful periods (such as fever, trauma, infection, or surgery).

If you want to achieve most effective results do not stop taking Generic Precose suddenly.

Overdose

If you overdose Generic Precose and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature below 25 degrees C (77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Precose are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Precose if you are allergic to Generic Precose components.

Be careful with Generic Precose if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Generic Precose if you have blockage of the stomach or intestine or are at risk for these problems.

Do not take Generic Precose if you have long-term (chronic) bowel inflammation, colon ulcers, or stomach or intestine problems that interfere with digestion or nutrient absorption.

Do not take Generic Precose if you have cirrhosis of the liver or unexplained abnormal liver function tests.

Do not take Generic Precose if you have diabetic ketoacidosis (high ketone levels) or severe kidney problems.

Try to be careful with Generic Precose if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Try to be careful with Generic Precose if you have allergies to medicines, foods, or other substances

if you have stomach or intestinal problems, liver problems, or kidney problems.

Try to be careful with Generic Precose if you are taking anticoagulants (eg, warfarin) because the risk of their side effects, including bleeding, may be increased by Generic Precose; calcium channel blockers (eg, verapamil), corticosteroids (eg, prednisone), diuretics (eg, hydrochlorothiazide), estrogen, isoniazid, nicotinic acid, oral contraceptives (birth control pills), phenothiazines (eg, chlorpromazine), phenytoin, sympathomimetics (eg, pseudoephedrine), or thyroid hormone because they may increase or decrease Precose 's effectiveness; insulin or sulfonylureas (eg, glyburide) because the risk of their side effects may be increased by Generic Precose; digoxin because its effectiveness may be decreased by Generic Precose.

Avoid alcohol.

Do not stop taking Generic Precose suddenly.

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A retrospective cohort study using the Taiwan National Health Insurance claims database was conducted to examine the risks of HHF among newly diagnosed type 2 diabetic patients who initiated glinide, sulfonylurea, or acarbose therapy during 2006-2012. The outcome of interest was hospitalization due to heart failure after treatment initiation, defined by ICD-9-CM code. A Cox proportional hazard regression model was used to calculate the hazard ratio (HR) and 95% confidence interval (CI) using acarbose as the reference group.

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Glimepiride was associated with a significantly greater responder rate than acarbose (61 vs 34%, p < 0.001), significantly greater decreases in HbA1c (2.5 +/- 2.2% vs 1.8 +/- 2.2%, p = 0.014) and FBG (2.6 +/- 2.6 mmol/l vs 1.4 +/- 2.8 mmo/l, p = 0.004), a decreased glucose response to breakfast compared with acarbose [area under curve (AUC) end: 8.9 +/- 2.7 mmol/l vs 11.3 +/- 3.9 mmol/l, p = 0.0001], and was accompanied by significantly greater compliance (91 < or = 12% vs 66 +/- 26%, p = 0.0001). Weight loss during the study was observed in both the acarbose group (1.9 +/- 3.9 kg, p = 0.001) and glimepiride group [0.4 +/- 5.2 kg, p = 0.8 (NS)].

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Acarbose slows progression of IMT in IGT subjects, a high-risk population for diabetes and atherosclerosis. This is the first placebo-controlled prospective subgroup analysis, demonstrating that counterbalancing of postprandial hyperglycemia may be vasoprotective.

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An analytical method for quantifying underivatized amino acids (AAs) in urine samples of rats was developed by using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Classification of type 2 diabetes rats was based on urine amino acids metabolic profiling. LC-MS/MS analysis was applied through chromatographic separation and multiple reactions monitoring (MRM) transitions of MS/MS. Multivariate profile-wide predictive models were constructed using partial least squares discriminant analysis (PLS-DA) by SIMAC-P 11.5 version software package and hierarchical cluster analysis (HCA) by SPSS 18.0 version software. Some amino acids in urine of rats have significant change. The results of the present study prove that this method could perform the quantification of free AAs in urine of rats by using LC-MS/MS. In summary, the PLS-DA and HCA statistical analysis in our research were preferable to differentiate healthy rats and type 2 diabetes rats by the quantification of AAs in their urine samples. In addition, comparing with health group the seven increased amino acids in urine of type 2 rats were returned to normal under the treatment of acarbose.

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A model was developed to simulate the course of individuals with IGT under each treatment strategy. Patients remain in the IGT state or transition from IGT to diabetes, to normal glucose tolerance (NGT) or to death. Effectiveness and resource use data were derived from published intervention trials. A comprehensive health-care payer perspective incorporating all major direct costs, reported in 2000 Canadian dollars, was adopted.

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Tendencies in the consumption of antidiabetic agents in Andalusia between 1986-1994 were analysed, with special emphasis on the impact of the introduction of acarbose and mechanized systems for the injection of insulin.

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The use of a single dose of 100 mg acarbose at breakfast time can result in a marked flattening of elevated post-prandial morning blood glucose profiles in both insulin-dependent type II and type I diabetics.

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The fermentation of starch in vitro produces a higher proportion of butyrate than the fermentation of most other substrates. The alpha-glucosidase inhibitor acarbose increases the amount of starch entering the colon, and has been shown to increase faecal butyrate in humans. It is generally considered that colonic butyrate is quantitatively removed by the colonic mucosa and liver and does not appear in peripheral blood. However, studies in animals suggest that a small proportion of colonic butyrate reaches peripheral blood. Thus, we hypothesised that an increase in colonic butyrate production would result in a rise in serum butyrate in human subjects. To test this, subjects with impaired glucose tolerance were randomly treated in a double-blind fashion with placebo (n 11) or acarbose (n 11) (100 mg three times per day). Serum short-chain fatty acid concentrations were measured twelve times over 12 h with subjects eating a standard diet before randomization and after 4 months of therapy. At baseline, 12 h mean serum butyrate concentrations were similar in the placebo and acarbose groups (2.8 (SE 0.7) and 3.3 (SE 0.6) microM, respectively). After 4 months on placebo, mean serum butyrate (2.6 (SE 0.5) microM) was no different from baseline. However, after 4 months on acarbose, serum butyrate had increased to 4.2 (SE 1.0) microM, a value which differed significantly from both the baseline value in the acarbose group and the treatment value in the placebo group. We conclude that acarbose increased serum butyrate in subjects with impaired glucose tolerance. These results support the hypothesis that increased colonic butyrate production in human subjects can be detected by an increase in serum butyrate.

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Dumping syndrome and postprandial hypoglycemia have been reported after Nissen fundoplication. The physiopathologic mechanisms are poorly understood and a variety of therapies have failed to control the hypoglycemia in these patients. We report a series of 6 infants with postprandial hypoglycemia after Nissen fundoplication who were treated successfully with acarbose.

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Two hundred twelve obese subjects with NIDDM who had not received any diabetic medication for at least 12 weeks were randomized to receive acarbose or placebo. The subjects were stratified by fasting glucose level above or below 11.1 mmol/L (200 mg/dL). Based on the subject's therapeutic response and tolerance, the acarbose dosage was titrated from 50 to 300 mg three times per day. This 36-week study consisted of a 6-week pretreatment period, a 24-week double-blind treatment period, and a 6-week posttreatment period.

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To assess the efficacy of acarbose monotherapy during 12-weeks treatment on the fasting glycemic level, lipid and lipoproteins profiles, in patients with type 2 diabetes mellitus.

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Twelve patients with non-insulin-dependent diabetes mellitus (NIDDM) and ten healthy volunteers were studied. Three meal tests with an intake of 90 g of white bread (50 g of carbohydrates) were performed on each subject. In one test, 200 mg of acarbose was given, while 15 g of P. psyllium mucilage was given in another test, and only bread was ingested in the control test. Serum glucose and insulin concentrations were measured every 30 min from 0-180 min. Net area under curve (AUC) concentrations of glucose and insulin, GI and insulinic index were calculated.

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Three groups of compounds were isolated in this study (triterpenes, flavonols and dithiolanes). Triterpenes and flavones showed activity in at least one bioassay (antiparasitic or α-glucosidase). In addition, only the pentacyclic triterpenes exhibited a competitive type of inhibition against α-glucosidase.

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Glucosidase activity was assayed at PH optima by PNPG substrate. Lobster sauce extracts were prepared by soaking, centrifagation. Polysaccharide were prepared by soaking, centrifagation, separation.

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Ascophyllum nodosum is a brown seaweed that grows abundantly in the Northeast coastal region. In this study, the potential of A. nodosum for type 2 diabetes management through antioxidant-mediated alpha-glucosidase and alpha-amylase inhibition was investigated. After the initial screening of 4 locally harvested seaweeds, A. nodosum was chosen for its highest phenolic content and was subjected to water extraction. Among extraction ratios of 50 g to 100 to 1000 mL at room temperature, 50 g/400 mL yielded the highest phenolic content of 4.5 mg/g wet weight. For evaluation of extraction temperature ranging from 20 to 80 degrees C, 50 g/400 mL was chosen as a minimum amount of extractant. Among temperatures studied, extraction at 80 degrees C resulted in the highest total phenolic contents (4.2 mg/g wet weight). All extracts had similar levels of antioxidant activity in the range of 60% to 70% in terms of 1, 1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity. The 80 degrees C extract had the highest alpha-glucosidase and alpha-amylase inhibitory activity with IC(50) of 0.24 and 1.34 microg phenolics, respectively, compared to the IC(50) of acarbose, reference inhibitor, being 0.37 and 0.68 microg. The results show that fresh A. nodosum has strong alpha-glucosidase and mild alpha-amylase inhibitory activities that correlated with phenolic contents. This study suggests a nutraceutical potential of A. nodosum based on phytochemical antioxidant and antihyperglycemia activities.

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Since ages, botanical substances are in use for the remedy of diabetes with considerable degree of success. One of the such; an extract of Commelina communis L. (CE-L) after decoction in water has been traditionally used for the treatment of diabetes in Korea. However, its action mechanism has not yet been established. To explore the inside of its action-mechanism, in this study, the effect of the aqueous extract of C. communis L. (CE-L) on the activity of alpha-glucosidase was evaluated in vitro and in vivo. Aqueous extract of CE-L showed inhibitory activity of the alpha-glucosidase in a dose-dependent manner, in vitro. CE-L also seems to be by and large free from exerting any cytotoxic effect at least in CHO-K1 fibroblast and 3T3-L1 adipocyte. CE-L alleviated hyperglycemia caused by maltose or starch loading in normal and Streptozotocin (STZ)-induced diabetic mice with better efficacy than that of acarbose. In addition, prolonged administration of CE-L tends to normalize hyperglycemia in STZ-induced diabetic mice. Such results suggest that inhibitory activity of CE-L on alpha-glucosidase may contribute to delay in carbohydrate digestion and glucose absorption. Thus, CE-L has potential for use in the management of non-insulin-dependent diabetes.

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Context 3β-Acetoxyurs-11-en-13β,28-olide (I), a triterpenoid, is found in most plant species. Pharmacologically triterpenes are very effective compounds with potent anticancer, anti-HIV and antimicrobial activities. Objectives Microbial transformation of 3β-acetoxyurs-11-en-13β,28-olide (I) was performed in order to obtain derivatives with improved pharmacological potential. Materials and methods Compound (I, 100 mg) was incubated with Aspergillus niger culture for 12 d. The metabolite formed was purified through column chromatography. Structure elucidation was performed through extensive spectroscopy (IR, MS and NMR). In vitro α- and β-glucosidase inhibitory, and antiglycation potentials of both substrate and metabolite were evaluated. Results Structure of metabolite II was characterized as 3β-acetoxyurs-11,12-epoxy-13β,28-olide (II). Metabolite II was found to be an oxidized product of compound I. In vitro α- and β-glucosidases revealed that metabolite II was a potent and selective inhibitor of α-glucosidase (IC50 value = 3.56 ± 0.38 μM), showing that the inhibitory effect of metabolite II was far better than compound I (IC50 value = 14.7 ± 1.3 μM) as well as acarbose (IC50 value = 545 ± 7.9 μM). Antiglycation potential of compound II was also high with 82.51 ± 1.2% inhibition. Thus, through oxidation, the biological potential of the substrate molecule can be enhanced. Conclusion Biotransformation can be used as a potential tool for the production of biologically potent molecules.

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Many investigations have revealed that a certain concentration of osmolality was indispensable for efficient acarbose production, but little information was available on the response mechanism of acarbose-producing strains to osmotic stress. By using the gas chromatography-mass spectrometry (GC-MS) analysis coupled with the enzyme activity determination of central carbon metabolism, the present work investigated the metabolic characteristics of industrial acarbose-producing Actinoplanes sp. A56 under various osmolality levels. Relatively high osmolality (450-500 mOsm/kg) appeared to favor efficient acarbose production by Actinoplanes sp. A56, although it inhibited cell growth. Further GC-MS analysis showed that fatty acids were the uppermost differential intracellular metabolites under various osmolality levels, and the relatively high osmolality resulted in increases in levels of fatty acids.

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This study describes the derivatization of the pseudooligosaccharide acarbose and its main metabolite, component 2, with 7-aminonaphthalene-1,3-disulfonic acid (ANDS) in human urine. Their efficient separation was possible by means of capillary zone electrophoresis, using a capillary tube of fused-silica containing 100 mM triethylammonium phosphate buffer, pH 1.5. On column laser-induced fluorescence allowed the detection of the pseudooligosaccharides in human urine in the nanomolar range. With this method, acarbose and component 2 were quantified in human urine after application of 300 mg of acarbose.

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Although acarbose-induced hepatotoxicity appears to be uncommon, diabetic patients receiving long-term acarbose therapy should be closely monitored for this adverse effect.

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An anonymous questionnaire was used in two centres to assess knowledge about oral agents amongst 261 patients with Type 2 diabetes mellitus (mean age 64 years) and 102 health professionals (including doctors, nurses and pharmacists).

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The study was undertaken to assess the efficacy guargum, Acarbose and their combination in modifying the sucrose absorption in patients of non Insulin dependent diabetes mellitus (NIDDM). Fifty patients of NIDDM were randomly distributed in three groups. Group A had 20 patients who received 20 grams of guargum, Group B had 10 patients who received 100 mg of Acrabose, Group C had 20 patients who received 10 grams of guargum and 50 grams of Acrabose. All the patients underwent 50 grams sucrose tolerance test with and without the trial drugs. Blood glucose levels were determined at 0, 30, 60, 90 and 120 minutes after sucrose loading. With the drugs, there was a significant decrease in the blood glucose levels at all time intervals (p < 001) in all the three groups. In all the three groups the blood glucose levels with the trial drugs was significantly lower (p < 001) than without the drug. It was seen that acarbose alone and guargum alone did not differ significantly in reducing the blood sugar level whereas combination of two produced significantly greater reduction in blood glucose levels than either of the drug used alone. Thus both guargum and acarbose are equally effective in modifying the absorption of sucrose. When combined in half the dosage they have synergistic effect and the reduction in blood glucose level is greater than either of the drug used alone.

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Obesity and the onset of diabetes are two closely linked medical complications prevalent globally. Postprandial hyperglycemia is one of the earliest abnormalities of glucose homeostasis associated with type 2 diabetes (T2D). Postprandial glucose levels can be regulated through α-glucosidase inhibition. The present study aims to demonstrate the potent inhibitory role of naringenin against α-glucosidase activity. The mode of inhibition of naringenin was examined by measuring enzyme activity in vitro with different concentrations of substrate using Lineweaver-Burk plot analysis. It shows competitive inhibition towards mammalian α-glucosidase thereby competing with α-limit dextrins and oligosaccharide residues for binding in the active site. Similar results have been obtained from the molecular docking analyses, where naringenin shows preferential binding for the active sites in each of the evaluated human intestinal α-glucosidase enzymes. Post-docking intramolecular hydrogen bonding analysis shows water molecule mediated hydrogen bonding for N-terminal maltase glucoamylase and N-terminal sucrase isomaltase. Naringenin's docked pose in the C-terminal maltase glucoamylase active site does not show any particular water mediated interaction similar to the co-crystallized acarbose. Further, our results suggest that naringenin (25 mg/kg) exerts significant inhibition of intestinal α-glucosidase activity in vivo thereby delaying the absorption of carbohydrates in T2D rats, thus resulting in significant lowering of postprandial blood glucose levels. Both in vitro and in vivo results were compared to the commercially available α-glucosidase inhibitor acarbose. Our findings clearly indicate that naringenin dampens postprandial glycemic response and offers a potential complementary approach in the management of T2D.

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Noninsulin-dependent diabetes mellitus is a genetically determined form of diabetes, due to impaired insulin secretion by the B-cells as well as to insulin resistance of the peripheral tissues. According to the glucose toxicity theory hyperglycemia and hyperinsulinemia exist in a vicious circle. Therefore, it is a major therapeutical aim to put the B-cell to rest and improve insulin sensitivity by a strict control of fasting blood glucose and of postprandial hyperglycemia. Furthermore, associated abnormalities within the metabolic syndrome, such as hypertension, dyslipoproteinemia and hemostatic disorders should be corrected to avoid vessel complications. Therefore, it should be started with basic measures as body weight reduction, carbohydrate-rich and fat-poor diet and exercise. If these measures fail to achieve acceptable glycemic control, antihyperglycemic drugs (acarbose, metformin) are indicated, eventually in a combination with small doses of short-acting sulfonylureas. Further impairment of insulin secretion is the indication for sulfonylurea and/or insulin application. HbA1c of 7 to 7.5% should be the goal of antidiabetic therapy, also for patients in advanced age. The main criterion for the choice of antidiabetics is the present insulin secretion capacity. Simple indicators in this respect are changes of body weight, plasma triglycerides and C-Peptide after i.v. glucagon stimulation. Application of insulin in combination with other antidiabetics or in the form of intensified insulin therapy should not be too much postponed.

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To investigate the therapeutic effects of methanol extract of Citrus macroptera Montr.fruit in α-amylase inhibitory activity (in vitro) and hypoglycemic activity in normal and glucose induced hyperglycemic rats (in vivo).

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Despite abundant research that has been carried out on the potential health benefits of pu-erh tea, no consensus till now, has been reached on which constituent is mainly responsible for its bioactivity. In this work, the aqueous extract (AE) and its fraction enriched with active constituents were prepared from pu-erh tea, and their bioactivities were investigated. It was found that tea polyphenols (TP), tea polysaccharides (TPS), caffeine (Caf), protein (Pro), amino acids (AA) were accumulated in several fractions after solvent extraction despite not being separated completely. Meanwhile, 95% ethanol precipitate (EP) and ethyl acetate fraction (EF) possessed remarkable antioxidant activity and potent inhibitory effects against α-glycosidase in vitro. Furthermore, all the extracts (50 mg/kg BW) showed a significant (p<0.05) effect on postprandial hyperglycemia in diabetic mice as compared with a model group, and the suppression of EP was not significantly (p>0.05) different from that of acarbose at the same dosage (50 mg/kg BW), which indicate that these fractions could be developed as potential anti-diabetic agents.

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A cross-sectional and analytic study was conducted in Mexico City.

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Digoxin has a narrow therapeutic margin and potentially life-threatening cardiac adverse effects. Gastrointestinal disorders, neuropsychological disorders and bradycardia are warning signs. Some drug combinations can aggravate the cardiac adverse effects of digoxin, or reduce its efficacy. We reviewed the literature, using the standard Prescrire methodology, in order to examine which drugs are involved in these interactions, and the mechanisms involved. Most relevant data are based on small pharmacokinetic studies or detailed case reports. The adverse effects of digoxin are potentiated by renal impairment, which may be pre-existing or due to nephrotoxic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin-converting-enzyme (ACE) inhibitors, angiotensin II receptor antagonists and ciclosporin. Some coadministered drugs such as macrolides and cardiovascular drugs (especially amiodarone) can cause digoxin overdose through pharmacokinetic interactions. The mechanism most often implicated is inhibition of P-glycoprotein, of which digoxin is a substrate. Hypercalcaemia and hypokalaemia inducing drugs, heart-rate lowering drugs, and drugs that prolong the QT interval or slow cardiac conduction can potentiate the cardiac adverse effects of digoxin. Plasma concentration of digoxin is not affected. Several drugs, including sucralfate, acarbose, cytotoxic agents, and enzyme inducers, can reduce digoxin plasma concentrations. This effect is attributed to decreased gastrointestinal absorption or increased elimination of digoxin. In practice, patients treated with digoxin, and their caregivers, should be aware that digoxin has a narrow therapeutic margin and frequent and potentially severe adverse effects. Close clinical monitoring is necessary to detect early warning signs (bradycardia and gastrointestinal or neurological disorders). Digoxin assay alone is not always sufficient. Special care is required for patients with renal failure, the elderly and patients receiving potentially interacting drugs.

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Blood was drawn from 24 subjects (14 male, 10 female, age: 50.7 ± 7.36 years, BMI: 26.64 ± 3.38 kg/m2, GHbA1c: 7.00 ± 0.74%) with drug-naïve T2D at 0 and 120 min following a standard mixed meal for the measurements of active GLP-1, NO and NOS. The CIMT was measured prior to and following 24 weeks of acarbose monotherapy (mean dose: 268 mg daily).

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precose tabs 2016-11-19

Glycogen storage diseases (GSD) are inborn errors of glycogen metabolism. Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have buy precose been reported for GSD I (glucose-6-phosphatase deficiency) in the mouse, for GSD II (acid alpha-glucosidase deficiency) in the dog, in cattle and in the quail, for GSD III (debrancher enzyme deficiency) in the dog and for GSD VIII (phosphorylase kinase deficiency) in the rat and the mouse. Experimentally induced GSD-like conditions have been described in the rat (Acarbose-induced GSD II-like conditions, iodoacetate-induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A-induced symptoms of cyclic AMP-dependent protein kinase deficiency). Enzymatic defects that are typical of the human GSD types have not been clearly identified in the induced animal conditions. The homology of animal and human GSD types is discussed. It is concluded that clinical, pathogenic and therapeutic studies of GSD may benefit from the use of animal models. For genetic studies of human GSD these models may prove to be of limited value, as the picture of several human GSD types is already obscured by genetic heterogeneity.

precose 25 mg 2017-01-08

Securidaca inappendiculata Hassk. (SI) is used to cure fractures and buy precose rheumatoid arthritis in China. Also, it is a potential antidiabetes drug; however, there are no reports on this.

precose online 2016-09-13

The effect buy precose of acarbose on the intestinal metabolism of glucose was investigated using an in vitro perfused preparation of the isolated rat small intestine-pancreas. In preparations perfused without intraluminal sucrose administration, the total glucose recovered in the portal effluent and the portal values of lactate, pyruvate and alanine did not depend on whether or not acarbose [1.5 mg/kg body weight (b.w.)] was present in the intestinal lumen. The intestinal glucose and lactate contents were very low at the end of the experiment, and identical with or without acarbose. Insulin and glucagon concentrations remained constant during the whole perfusion period. After intraluminal administration of sucrose a clear increase in portal glucose concentration was observed, which was severely reduced by acarbose administration no changes in portal levels of lactate, pyruvate, alanine, insulin and glucagon were observed. The intestinal content of sucrose at the end of the study was significantly higher in the presence of acarbose (1.5 mg/kg b.w.), while the glucose concentration was low both with and without acarbose (0.20 +/- 0.08 vs 0.29 +/- 0.09 mmol/l respectively). These results suggest that acarbose does not influence the metabolic utilization of the glucose being translocated from the lumen.

buy precose online 2016-06-14

To compare the efficacy of buy precose acarbose and metformin in overweight and/or obese patients with newly diagnosed type 2 diabetes mellitus (T2DM).

precose user reviews 2017-07-28

Investigate the hypoglycaemic activity of the four isolated compounds from a crude acetone extract of the root bark of Euclea undulata var. myrtina, which is used by buy precose traditional healers in the Venda area, Limpopo Province in the treatment of diabetes.

precose 100 mg 2017-12-19

The WDF rats exhibit higher body weight and fasting blood glucose, insulin, triglyceride and cholesterol concentrations compared to lean animals. Moreover, they show marked glucose intolerance as indicated by the glucose and insulin excursions during OGTT. Interestingly, in both treated and untreated animals, a reversion of the hyperglycaemic state as well as an improvement of the buy precose glucose tolerance is observed. However, whereas in the group receiving no acarbose this is accounted for by dramatic increases in fasting plasma insulin concentrations and insulin secretion during OGTT (as indicated by the DeltaInsulin area), in rats treated with acarbose the reversion of the diabetic state takes place without increments in hormone concentration. In addition, rats treated with acarbose for 3.5 and 7.5 months show lower plasma triglyceride and FFA concentrations, and the same was observed for cholesterol at the highest dosage of the drug.

precose medication 2017-09-19

The present buy precose study investigated the effect of acarbose on insulin requirements and glycaemic control in patients with type 2 diabetes receiving exogenous insulin due to secondary failure of maximum dose sulphonylurea therapy.

precose dosing 2016-12-03

In older patients with type 2 diabetes, life expectancy and the presence of microvascular complications determine the appropriate intensity of glucose control. The available antidiabetic agents offer many options for achieving glycemic targets, based on the needs of the individual patient. New stimulators of insulin secretion include glimepiride (a sulfonylurea) and repaglinide (a meglitinide). The biguanide metformin is especially useful in obese, insulin-resistant patients. Alpha-glucosidase inhibitors such as acarbose and miglitol act locally in the GI tract to reduce postprandial excursion in glucose levels. The insulin-sensitizing drug buy precose troglitazone enhances insulin-mediated glucose disposal. When troglitazone is used, careful monitoring of patients' liver function is required.

precose dosage 2016-02-12

MEDLINE, DARE, and the Cochrane Database of buy precose Systematic Reviews were searched to identify published systematic reviews as a source for trials.

acarbose precose medication 2015-07-11

Although natural substrates of glycosidase are polysaccharides, in buy precose the present study we successfully isolated novel peptide modulators of alpha-glucosidase. Modulatory activity of selected peptides could be further optimized through peptidomimetic design. They represent promising leads for development of efficient alpha-glucosidase inhibitors.

precose generic name 2016-03-12

Nine patients with Type 2 diabetes receiving insulin therapy were treated with acarbose 100 mg thrice daily for 1 week to investigate the effect of acarbose on blood glucose control. Daily blood glucose profiles contained fewer excursions during acarbose administration and low levels were maintained. The M-value, an indicator of blood glucose fluctuation, decreased significantly from a run-in period value of 37.6 +/- 8.7 (SEM) to 16.7 +/- 4.0 during the acarbose period (p < 0.05) and rose again to 28.9 +/- 6.7 (p > or = 0.05) in the follow-up period. The 24-h urinary glucose excretion similarly decreased during acarbose administration. As expected, no decrease in HbA1C was observed due to the short treatment period. The 24-h urinary C-peptide excretions and serum lipids were not influenced by acarbose therapy. Frequent episodes of clinical hypoglycaemia were experienced while on acarbose therapy, indicating a decrease in insulin requirements. Adverse events such as flatulence and abdominal distention were buy precose observed in six out of nine cases. Symptoms were generally mild and well tolerated, only one patient dropped out because of diarrhoea and abdominal pain. We conclude that acarbose could usefully be administered to Type 2 diabetic patients treated with insulin to improve blood glucose control and reduce insulin requirement if the appropriate selection criteria were met.

precose dose 2017-06-02

To study the impact of starch malabsorption on fecal short-chain fatty acid concentrations, 11 healthy volunteers consumed a controlled diet rich in starch for 2 4-week periods buy precose . They received the glucosidase inhibitor acarbose (Bay g 5421) in one of the study periods and placebo in the other. Stool wet weight increased by 68% and stool dry weight by 57% with acarbose. The fecal concentration (mumol/g wet weight) of n-butyrate (+58%) rose significantly when acarbose was added to the diet. The fecal excretion (mmol/day) of total short-chain fatty acids (+95%) and of their constituents acetate (+97%) and n-butyrate (+182%) was significantly higher when starch malabsorption was induced by acarbose.

precose tablets 2017-07-17

The frequency of type 2 diabetes mellitus is increasing at an alarming rate. Prediabetes, also referred to as impaired glucose tolerance (IGT) and/or impaired fasting glucose, is a major risk factor for development of type 2 diabetes mellitus. In addition, IGT has been associated with an increased risk of cardiovascular disease and mortality. Several studies have measured the effects of various interventions in patients with IGT on the development of type 2 diabetes mellitus. Intensive lifestyle modifications through alterations in diet and improvement in exercise have delayed the development of buy precose type 2 diabetes mellitus by 58% in patients with IGT. Therapy with metformin, troglitazone, or acarbose also has reduced the progression of IGT to diabetes mellitus by 31%, 49% and 25%, respectively. The mechanisms by which lifestyle interventions and drugs reduce the progression may be through alterations in insulin sensitivity. The American Diabetes Association recommends screening for prediabetes in patients who are 45 years or older and those with a body mass index of 25 kg/m2 or greater who have additional diabetes mellitus risk factors. Pharmacists can promote awareness, counsel patients on intervention strategies to delay the onset of diabetes mellitus, and screen high-risk patients.

precose cost 2015-11-27

This review, primarily for general readers, briefly presents experimental approaches to therapeutics of cancer, HIV/AIDS and various other diseases based on advances in buy precose glycobiology and glycochemistry. Experimental cancer and HIV/AIDS vaccines are being developed in attempts to overcome weak immunological responses to carbohydrate-rich surface antigens using carriers, adjuvants and novel carbohydrate antigen constructs. Current carbohydrate-based vaccines are used for typhus, pneumonia, meningitis; vaccines for anthrax, malaria and leishmaniasis are under development. The link between O-linked beta-N-acetylglucosamine glycosylation and protein phosphorylation in diseases including diabetes and Alzheimer's disease is also explored. Carbohydrate-associated drugs that are in current use or under development, such as heparan sulfate binders, lectins, acarbose, aminoglycosides, tamiflu and heparin, and technologies using carbohydrate and lectin microarrays that offer improved diagnostic and drug development possibilities, are described. Advances in carbohydrate synthesis, analysis and manipulation through the emerging fields of glycochemistry and glycobiology are providing new approaches to disease therapeutics.

precose reviews 2016-04-22

The primary objective of this double-blind, placebo-controlled, randomised cross-over study was to investigate the influence of acarbose on insulin requirement in patients with Type 1 diabetes (T1DM) following a standardised meal. In addition, the study assessed the effects of acarbose on post-prandial triglyceride, glucagon and gastrointestinal peptide levels, gastric emptying, and oxidative glucose metabolism. Following normalisation of their blood glucose, 10 patients received a standardised meal together with acarbose (100 mg) or placebo. Each patient was evaluated twice (separated by 10+/-3 days), and the cross-over study design ensured that they received both acarbose and placebo. The insulin requirement for maintenance of normoglycaemia was assessed using a closed-loop insulin infusion system (artificial pancreas, Biostator). Acarbose produced a statistically significant reduction in mean insulin requirement over a 3-hr period following the meal compared with placebo (5171.7+/-2282.6 mU vs 8074.5+/-3045.4 mU; p=0.003). The level of blood glucose control over the same period was similar in the two groups. Gastric inhibitory polypeptide levels also showed a statistically significant decrease with acarbose treatment compared with placebo for AUC (area under the curve; p=0.006) and Cmax (maximum plasma concentration; p=0.022), but not tmax (time to reach Cmax from the start of the standardised meal; p>0.05). Analysis of the other efficacy parameters revealed no statistically significant differences between acarbose treatment Glucophage Dosage and placebo (p>0.05). These results indicate that acarbose decreases insulin requirement in patients with T1DM without affecting gastric emptying.

precose tablet 2015-07-10

A series of novel tetracyclic oxindole derivatives were synthesized via tandem Suzuki coupling-Michael addition reaction catalyzed by palladium. Twenty derivatives were designed and synthesized in 6-8 steps in 8-20% overall yields. Their structures were confirmed by (1)H, (13)C NMR and LC/MS. These compounds were evaluated for α-glucosidase inhibitory activity in vitro. Compounds 7c, 7d, 7e, 7g, 7h, and 7i exhibited IC50 values of 32.3, 12.1, 15.7, 29.0, 16.0, and 4.8 μM, respectively, with potency all higher than that of the control standard acarbose (IC50=115.8 μM). Molecular docking studies revealed the existence of potential hydrogen bonding and hydrophobic interaction between the enzyme and the active Naprosyn Prescription Dosage compound 7i.

precose buy 2017-10-25

Plasma MR- proANP and CT-proET-1 concentrations, but not MR-prADM concentrations, were affected by treatment with acarbose Pamelor Reviews over 12 weeks. Our findings provide new possible mechanisms of acarbose action in diabetes and metabolic syndrome.

precose drug 2015-06-20

Non-insulin-dependent diabetes mellitus (type 2 diabetes) not responding to dietary treatment alone in patients with non- Best Luvox Dosage alcoholic liver cirrhosis is characterized by high postprandial hyperglycaemia. The control of postprandial hyperglycaemia in such patients, is generally achieved by the means of progressively higher doses of insulin, with an increasing risk of hypoglycaemia in the late postprandial period. The aim of this study was to evaluate the use of acarbose for the control of postprandial hyperglycaemia in 100 patients with well-compensated liver cirrhosis and type 2 diabetes treated with insulin.

precose drug interactions 2015-04-01

Thermococcus litoralis 4-alpha-glucanotransferase (TLGT) belongs to glucoside hydrolase family 57 and catalyzes the disproportionation of amylose and the formation of large cyclic alpha-1,4-glucan (cycloamylose) from linear amylose. We determined the crystal structure of TLGT with and without an inhibitor, acarbose. TLGT is composed of two domains: an N-terminal domain (domain I), which contains a (beta/alpha)7 barrel fold, and a C-terminal domain (domain II), which has a twisted beta-sandwich fold. In the structure of TLGT complexed with acarbose, the inhibitor was bound at the cleft within domain I, indicating that domain I is a catalytic domain of TLGT. The acarbose-bound structure also clarified that Glu123 and Asp214 were the catalytic nucleophile and acid/base catalyst, respectively, and revealed the residues involved in substrate binding. It seemed that TLGT produces large cyclic glucans by preventing the production of small cyclic glucans by steric hindrance, which is achieved by three lids protruding into Tegretol 100 Mg the active site cleft, as well as an extended active site cleft. Interestingly, domain I of TLGT shares some structural features with the catalytic domain of Golgi alpha-mannosidase from Drosophila melanogaster, which belongs to glucoside hydrolase family 38. Furthermore, the catalytic residue of the two enzymes is located in the same position. These observations suggest that families 57 and 38 evolved from a common ancestor.

precose drug class 2016-10-18

To gain an insight into a mechanism whereby maltitol increases intestinal absorption of calcium, we evaluated transepithelial calcium transport of everted segments of rat small intestine by comparing the values in the presence of maltitol with the values in the presence of maltose. In jejunal segments, no significant difference in the rate of calcium transport was seen between the incubations in the medium containing 100 mM maltitol and in the medium containing 100 mM maltose, regardless of the calcium concentrations in the mucosal-side medium. By contrast, the everted ileal segments incubated in the presence of maltitol exhibited two-fold greater transepithelial calcium transport than did the segments incubated in the presence of maltose at a high (10 mM) concentration of calcium, whereas at a low (0.5 mM) concentration of calcium, maltitol did not produce a significant effect. With the conditions in which intestinal alpha-glucosidases were inhibited using the medium containing Tris Neurontin Medication or acarbose, a slight (40%) but significant increase of calcium transport was again observed in the segments incubated in the medium containing maltitol as compared with the medium containing maltose. The results suggest that maltitol enhances the rate of transepithelial calcium transport in the lower part of small intestine by modulating the passive diffusion of calcium, and that not only the nature of low digestibility, but also some other nature(s) of maltitol might be responsible for the maltitol-induced increase of ileal calcium transport.

precose 50 mg 2015-11-07

Flow mediated vasodilation was improved and Flagyl Reviews progression of intima media thickness was reduced by acarbose. In the STOP-NIDDM trial in people with IGT acarbose decreased the incidence of diabetes by 36%. The STOP-NIDDM trial with CV events as secondary objective is the only intervention trial in people with IGT so far with a significant benefit for CV disease inclusive hypertension. In a metaanalysis of controlled studies (MeRIA) in patients with type 2 diabetes, treatment with acarbose was associated with a 64% lower rate of myocardial infarction and 35% less CV events.

precose patient review 2015-05-19

We conducted a nationwide, population-based study using a large cohort with diabetes in the Taiwan National Health Insurance Research Database. Patients with newly diagnosed diabetes (n = 1,343,484) were enrolled between 1998 and 2010. One control subject not using acarbose was randomly selected for each subject using acarbose after matching for age, sex, diabetes onset, and Augmentin 1000 Mg comorbidities. Cox proportional hazards regression with a competing risks analysis was used to calculate the hazard ratios (HRs) and 95% CIs for the association between acarbose use and incident colorectal cancer for each eligible case-control pair (n = 199,296).

precose drugs 2016-04-11

Insulin has been the mainstay of treatment of diabetes during pregnancy for decades. Although glyburide and metformin are classified as category B during pregnancy, recent research has suggested that these oral agents alone or in conjunction with Tegretol 2 Suspension insulin may be safe for the treatment of gestational diabetes (GDM). This paper summarizes the data on the use of glyburide and metformin for treatment of GDM.